The DOI matches its Crossref record; 50 of the 50 references it cites were found in a registry or an index; none of the 35 sources its claims cite is checked for support yet.
Abnormal sympathetic overactivity evoked by insulin in the skeletal muscle of patients with essential hypertension.
Open accessAbstract
The reason why hyperinsulinemia is associated with essential hypertension is not known. To test the hypothesis of a pathophysiologic link mediated by the sympathetic nervous system, we measured the changes in forearm norepinephrine release, by using the forearm perfusion technique in conjunction with the infusion of tritiated NE, in patients with essential hypertension and in normal subjects receiving insulin intravenously (1 mU/kg per min) while maintaining euglycemia. Hyperinsulinemia (50-60 microU/ml in the deep forearm vein) evoked a significant increase in forearm NE release in both groups of subjects. However, the response of hypertensives was threefold greater compared to that of normotensives (2.28 +/- 45 ng.liter-1.min-1 in hypertensives and 0.80 +/- 0.27 ng.liter-1 in normals; P less than 0.01). Forearm glucose uptake rose to 5.1 +/- .7 mg.liter-1.min-1 in response to insulin in hypertensives and to 7.9 +/- 1.3 mg.liter-1.min-1 in normotensives (P less than 0.05). To clarify whether insulin action was due to a direct effect on muscle NE metabolism, in another set of experiments insulin was infused locally into the brachial artery to expose only the forearm tissues to the same insulin levels as in the systemic studies. During local hyperinsulinemia, forearm NE release remained virtually unchanged both in hypertensive and in normal subjects. Furthermore, forearm glucose disposal was activated to a similar extent in both groups (5.0 +/- 0.6 and 5.2 +/- 1.1 mg.liter-1.min-1 in hypertensives and in normals, respectively). These data demonstrate that: (a) insulin evokes an abnormal muscle sympathetic overactivity in essential hypertension which is mediated by mechanisms involving the central nervous system; and (b) insulin resistance associated with hypertension is demonstrable in the skeletal muscle tissue only with systemic insulin administration which produces muscle sympathetic overactivity. The data fit the hypothesis that the sympathetic system mediates the pathophysiologic link between hyperinsulinemia and essential hypertension.
Overview
AI snapshot
Written from the paper’s full text.
TL;DR
In patients with essential hypertension, systemic euglycemic hyperinsulinemia evoked a threefold greater increase in forearm skeletal muscle norepinephrine release than in normotensive controls. Local intra-arterial insulin did not change norepinephrine release in either group, suggesting the abnormal sympathetic response is centrally mediated rather than a direct muscle effect.
Key findings
- Systemic insulin infusion increased forearm NE release in both groups, but the absolute rise was threefold higher in hypertensives (2.28±0.45 vs. 0.80±0.27 ng·liter⁻¹·min⁻¹; P < 0.01); percent increases were 140% in hypertensives (P < 0.001) and 35% in normotensives (P < 0.05).
- During systemic insulin, forearm glucose uptake was lower in hypertensives than normotensives (5.1±0.7 vs. 7.9±1.3 mg·liter⁻¹·min⁻¹; P < 0.05), and whole-body glucose utilization was also lower (4.6±0.3 vs. 5.8±0.5 mg/kg per min; P < 0.05).
- During local intrabrachial insulin, forearm NE release remained virtually unchanged in both groups, while forearm glucose disposal was similar in hypertensives and normals (5.0±0.6 and 5.2±1.1 mg·liter⁻¹·min⁻¹, respectively).
- Forearm NE balance increased fourfold in hypertensives during systemic hyperinsulinemia (P < 0.05), whereas it was statistically indistinguishable from zero in normals.
Methods
- Forearm perfusion technique with tritiated norepinephrine tracer was used in 45 subjects: 21 normotensives and 24 patients with mild to moderate essential hypertension.
- Two protocols: systemic insulin infusion at 1 mU/kg per min for 120 min with euglycemia (12 normals, 14 hypertensives), or local intrabrachial insulin at 0.05 mU/kg per min (9 normals, 10 hypertensives); tracer subgroups received [³H]norepinephrine.
- Forearm NE kinetics were calculated from arterial–venous balance, fractional extraction, clearance, uptake, and release; comparisons used paired and unpaired t tests, with values reported as mean±SE.
Limitations
- The paper states that it cannot answer whether hyperinsulinemia is the primary defect leading to hypertension via sympathetic overactivity, and that an alternative primary sympathetic overactivity causing both hypertension and insulin resistance would be equally compatible with the data.
- The paper states that the mechanism of insulin-evoked muscle sympathetic overactivity is unknown and that a peripheral reflex such as a venous baroreflex or chemoreflex cannot be excluded.
- Evident from the text: sample sizes are small, especially for tracer subgroups (e.g., 8 normals and 7 hypertensives for systemic tracer studies; 5 and 5 for local tracer studies), and the local infusion model relies on adequate mixing, which was assessed in only 16 tested cases.
Model-written summary. Check it against the paper before relying on it.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
0 of 35 cited sources checked · 0 supported · 0 flagged
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hyperinsulinemia (50-60 jsU/ml in the deep forearm vein) evoked a significant increase in forearm NE release in both groups of subjects.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Introduction
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Forearm glucose uptake increased in response to intraarterial insulin infusion to a comparable ex- tent in both groups.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The mean absolute change in forearm NE release during hyperinsulinemia was threefold higher in hypertensive (2.28±0.45ng.liter-' * min') than in normotensive subjects (0.80±0.27 ng liter-' * min-') (P < 0.01) (Fig. 1).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Arterial plasma FFA levels were not affected by local insulin (from 0.42±0.05 to 0.39±0.04mmol in normal sub- jects and from 0.36±0.05 to 0.39±0.05mmol in hypertensives).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“since blood pressure remained unchanged throughout insulin infusion.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Discussion
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“During local hyperinsulinemia, forearm NE release re- mained virtually unchanged both in hypertensive and in normal subjects.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Introduction
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Comparable values of NE fractional extraction and clearance were found during both the basal state and the hyperinsulin- emic period.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and did not change significantly during insu- lin infusion in both groups (Table II).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Arterial blood glucose levels remained unchanged in both groups during local, intrabrachial insulin infusion.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“During the hyperinsuline- mic period, forearm NE release increased significantly by 35% in normotensives (P < 0.05).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- It may state two separate claims as one. 17
- Probably not a substantial claim. 8
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Heart rate was comparable in the two groups in basal conditions and increased slightly during hyperinsulinemia only in hypertensive patients (P < 0.05).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In normal subjects, forearm NE balance was statistically indistinguishable from zero both in the basal state and during insulin infusion.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As expected, systolic and diastolic blood pressures were significantly higher in hypertensives than in normotensives”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Both forearm NE uptake and NE release were totally unaffected by local forearm insulinization.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Plasma insulin concentration in the deep forearm vein was similar in the basal state in the two groups and increased to a comparable extent during systemic insulin infusion.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Accordingly, forearm NE uptake was similar in the basal state and increased comparably in the two groups during insulin infusion (P < 0.05).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Forearm glucose uptake rose to 5.1±.7 mg * liter-' * min-in response to insulin in hypertensives and to 7.9±1.3mg.liter' -min' in normotensives (P < 0.05).”
- Also stated in: § Downers Grove, IL). · plain
“Forearm glucose uptake in the basal state was not statistically different in normal and hypertensive subjects and increased considerably in response to insulin infusion in both groups.However, the levels attained in hypertensive patients were significantly lower than those ob- served in control subjects (P < 0.05) (Table III).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Introduction
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Downers Grove, IL). · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Ve- nous plasma insulin levels increased to the same extent after insulin whereas systemic insulin concentration remained stable at its basal level.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As shown in Table III, basal arterial blood glucose concen- trations were similar in normal and hypertensive subjects, and remained virtually unchanged during insulin infusion in both groups.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Estimated forearm blood flow was similar in the two groups in the basal state and increased slightly but not signifi- cantly after insulin administration (Table III).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Downers Grove, IL).
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These data demonstrate that: (a) insulin evokes an ab- normal muscle sympathetic overactivity in essential hyperten- sion which is mediated by mechanisms involving the central nervous system;”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Introduction
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In this model, insu- lin resistance, hyperinsulinemia, and hypertension develop”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Introduction
What the sources say
- Not checked yetcites [5]
- Not checked yetcites [6]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Particularly relevant is the observation that a program of physical activity or body weight control leads to a parallel reduction of hyperinsulinemia and blood pressure levels (7).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Introduction
What the sources say
- Not checked yetcites [7]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This leads to the conclu- sion that all of the insulin effect on muscle NE metabolism, seen with systemic insulinization, is mediated either by central mechanisms involving the hypothalamic nuclei or by a periph- eral reflex.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Rests on an assumption: Forearm norepinephrine release measured by the [3H]norepinephrine infusion technique reflects skeletal muscle sympathetic nerve activity.
In the paper
“Of interest is also the recent observation that in the offspring of essential hyperten- sive parents insulin resistance and hyperinsulinemia are de- monstrable before the development of high blood pressure (8).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Introduction
What the sources say
- Not checked yetcites [8]
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“(d) sympathetic overactivity may be potentially responsible for elevated blood pressure (15)”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Introduction
What the sources say
- Not checked yetcites [15]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“Evi- dence to support this last hypothesis comes from the observa- tion that in vitro insulin affects NE uptake by the atrial strips (39).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Discussion
What the sources say
- Not checked yetcites [39]
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and (b) insulin resistance associated with hypertension is demonstrable in the skeletal muscle tissue only with systemic insulin administration which produces muscle sympathetic overactivity.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Introduction
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“and that NE can in- duce vascular smooth muscle cell polyploidy independent of blood pressure elevation (47).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Discussion
What the sources say
- Not checked yetcites [47]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Alternatively, the data may indicate that the exaggerated sympathetic activation induced by systemic insulinization in hypertensives may play a causal role in the impaired glucose uptake by the muscle tissue.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These are potential factors that may lead to structural alterations in the arterial vessels, thus reducing the lumen area, amplifying the vasoconstrictor re- sponse to contractile agents, and limiting vasodilation.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Whatever the initial event, our data also point out the possibility that the abnormal sympathetic response to insulin may further aggravate insulin resistance and hypennsu- linemia, thus acting as a self-perpetuating mechanism in essen- tial hypertension.”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“The different response of muscle glucose uptake to local or systemic insulin may suggest that muscle insulin resistance in hypertension is entirely mediated by the indirect component of insulin action (28).”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Discussion
What the sources say
- Not checked yetcites [28]
Tests✗ Asserted: fails✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. The authors may not put it forward as true.
None of the sources cited for this claim have been checked yet.
In the paper
“In this context, it is pertinent to recall that the sympa- thetic nervous system promotes the growth of vascular muscle fibers (43, 44) and myocardium (45,46)”
§ Abnormal Sympathetic Overactivity Evoked by Insulin in the Skeletal Muscle of Patients with Essential Hypertension > Discussion
What the sources say
- Not checked yetcites [43]
- Not checked yetcites [44]
- Not checked yetcites [45]
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
The reason why hyperinsulinemia is associated with essential hypertension is not known.
“The reason why hyperinsulinemia is associated with essential hypertension is not known.”
The paper relies on this without support.
The available clinical data support the concept that insulin and human hypertension must be linked by pathophysiologic mechanisms.
“The available clinical data, however, tend to support the concept that the two factors must be linked by pathophysiologic mechanisms.”
The paper relies on this without support.
The effluent venous blood from the deep antecubital vein drains predominantly muscle tissue.
“Under these conditions, the effluent venous blood drained predominantly muscle tissue.”
The paper relies on this without support.
Forearm norepinephrine release measured by the [3H]norepinephrine infusion technique reflects skeletal muscle sympathetic nerve activity.
“In conclusion, the current study provides evidence for an abnormal muscle sympathetic activity reflexly evoked by insu- lin in essential hypertension.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Euglycemic hyperinsulinemia evokes both sympathetic activation and vasodilation in skeletal muscle, but the mechanism remains unknown.”
From Differential effects of hyperinsulinemia and carbohydrate metabolism on sympathetic nerve activity and muscle blood flow in humans (1993) · cites this paper as [8]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Alternatively, a central neural action of insulin may also contribute to stimulation of sympathetic outflow in this setting (8, 40-43).”
From Differential effects of hyperinsulinemia and carbohydrate metabolism on sympathetic nerve activity and muscle blood flow in humans (1993) · cites this paper as [8]
The cited source says what the claim attributes to it.
In the citing paper
“findings in humans, showing that local intraarterial insulin infusion, in contrast to systemic intravenous infusion, did not have any stimulatory effect on sympathetic activity in skeletal muscle (15).”
From Impaired insulin-induced sympathetic neural activation and vasodilation in skeletal muscle in obese humans. (1994) · cites this paper as [15]
The cited source says what the claim attributes to it.
In the citing paper
“in hypertensive insulin-resistant humans, Lembo et al. (15) recently provided evidence for augmented stimulation of norepinephrine release into forearm tissue by insulin.”
From Impaired insulin-induced sympathetic neural activation and vasodilation in skeletal muscle in obese humans. (1994) · cites this paper as Lembo et al. (15)
In the citing paper
“In contrast, Lembo et al84 demonstrated that insulin-induced increases in sympathetic activity and norepinephrine release in skeletal muscle are substantially exaggerated in hypertensive patients (Figure 3, right panel).”
From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [84]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
NE-release calculation has its subtraction reversed
MinorUnder the paper's stated sign convention, net NE balance is uptake minus release. Release therefore equals uptake minus net balance, not net balance minus uptake as the calculation describes.
“Once FNU was calculated, forearm NE release was easily obtained by subtracting FNU from the net NE balance.”
“Positive or nega- tive balance values indicate uptake or release, respectively.”
Citations
Cites
Insulin Resistance in Essential Hypertension
Ferrannini, E., Buzzigoli, G., Bonadonna, R., Giorico, M. A., Oleggini, M., Graziadei, L., Pedrinelli, R., Brandi, L., & Bevilacqua, S. (1987) · New England Journal of Medicine · doi:10.1056/nejm198708063170605 · Cited by 2,344
Anton, A. H., & Sayre, D. F. (1962) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1016/s0022-3565(25)26438-2 · Cited by 2,261
Hyperinsulinemia. A link between hypertension obesity and glucose intolerance.
Modan, M., Halkin, H., Almog, S., Lusky, A., Eshkol, A., Shefi, M., Shitrit, A., & Fuchs, Z. (1985) · Journal of Clinical Investigation · doi:10.1172/jci111776 · Cited by 1,465
Desbuquois, B., & Aurbach, G. D. (1971) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-33-5-732 · Cited by 1,295
Effect of Insulin and Glucose Infusions on Sympathetic Nervous System Activity in Normal Man
Rowe, J. W., Young, J. B., Minaker, K. L., Stevens, A. L., Pallotta, J., & Landsberg, L. (1981) · Diabetes · doi:10.2337/diab.30.3.219 · Cited by 1,143
Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans.
Anderson, E. A., Hoffman, R. P., Balon, T. W., Sinkey, C. A., & Mark, A. L. (1991) · Journal of Clinical Investigation · doi:10.1172/jci115260 · Cited by 1,075
Fructose-induced insulin resistance and hypertension in rats.
Hwang, I. S., Ho, H., Hoffman, B. B., & Reaven, G. M. (1987) · Hypertension · doi:10.1161/01.hyp.10.5.512 · Cited by 885
Recommendations for Human Blood Pressure Determination by Sphygmomanometers
Kirkendall, W. M., Burton, A. C., Epstein, F. H., & Freis, E. D. (1967) · Circulation · doi:10.1161/01.cir.36.6.980 · Cited by 882
Anderson, E. A., Sinkey, C. A., Lawton, W. J., & Mark, A. L. (1989) · Hypertension · doi:10.1161/01.hyp.14.2.177 · Cited by 632
The Effect of Weight Loss on the Sensitivity of Blood Pressure to Sodium in Obese Adolescents
Rocchini, A. P., Key, J., Bondie, D., Chico, R., Moorehead, C., Katch, V., & Martin, M. (1989) · New England Journal of Medicine · doi:10.1056/nejm198908313210905 · Cited by 621
Flagged first, then by citations
Cited by
Sorted by citations
Items 101–200 of 252
McNally, P. G., Lawrence, I. G., Watt, P. A. C., Hillier, C., Burden, A. C., & Thurston, H. (1995) · Diabetologia · doi:10.1007/bf00410285 · Cited by 34
Kopp, W. (2018) · Nutrition and Metabolic Insights · doi:10.1177/1178638818773072 · Cited by 35
Lumiaho, A., Pihlajamäki, J., Hartikainen, J. E. K., Ikäheimo, R., Miettinen, R., Niemitukia, L. H., Lampainen, E., & Laakso, M. (2003) · American Journal of Kidney Diseases · doi:10.1016/s0272-6386(03)00354-8 · Cited by 33
Effect of Propolis on Insulin Resistance in Fructose-drinking Rats
Zamami, Y., Takatori, S., Koyama, T., Goda, M., Iwatani, Y., Doi, S., & Kawasaki, H. (2007) · YAKUGAKU ZASSHI · doi:10.1248/yakushi.127.2065 · Cited by 33
Limberg, J. K., Soares, R. N., & Padilla, J. (2022) · Current Diabetes Reports · doi:10.1007/s11892-022-01456-1 · Cited by 34
Forjaz, C. L. M., Ramires, P. R., Tinucci, T., Ortega, K. C., Salomão, H. E. M. H., Ignes, E. C., WAJCHENBERG, B. L., Negrão, C. E., & Mion, D. (1999) · Journal of Applied Physiology · doi:10.1152/jappl.1999.87.2.824 · Cited by 32
Takahashi, N., Anan, F., Nakagawa, M., Yufu, K., Shinohara, T., Tsubone, T., Goto, K., Masaki, T., Katsuragi, I., Tanaka, K., et al. (2007) · Metabolism · doi:10.1016/j.metabol.2007.02.005 · Cited by 31
Arauz-Pacheco, C., Lender, D., Snell, P. G., Huet, B. A., RAMIREZ, L., Breen, L., MORA, P., & Raskin, P. (1996) · American Journal of Hypertension · doi:10.1016/s0895-7061(96)00256-7 · Cited by 30
Takatori, S., Zamami, Y., Mio, M., Kurosaki, Y., & Kawasaki, H. (2006) · Hypertension Research · doi:10.1291/hypres.29.361 · Cited by 30
Pathogenesis and etiology of essential hypertension: role of dietary carbohydrate
Kopp, W. (2004) · Medical Hypotheses · doi:10.1016/j.mehy.2004.10.009 · Cited by 29
Laine, H. K., Knuuti, J. M., Ruotsalainen, U., Utriainen, T., Oikonen, V., Raitakari, M., Luotolahti, M., Kirvelä, O., Vicini, P., Cobelli, C., et al. (1998) · Circulation · doi:10.1161/01.cir.97.21.2146 · Cited by 29
Insulin stimulates epinephrine release under euglycemic conditions in humans
Tack, C. J., Lenders, J. W. M., Willemsen, J. J., van Druten, J. A. M., Thien, T., Lutterman, J. A., & Smits, P. (1998) · Metabolism · doi:10.1016/s0026-0495(98)90251-7 · Cited by 28
Alidu, H. W., Dapare, P. P. M., Quaye, L., Amidu, N., Bani, S. B., & Banyeh, M. (2023) · BioMed Research International · doi:10.1155/2023/8873226 · Cited by 34
The incidental relationship between serum ferritin levels and hypertension
Ryoo, J., Kim, S. Y., Oh, C., Park, S. K., Kim, E., Park, S.-J., Yu, J. I., Kim, M., Choi, Y., & Ko, T. S. (2014) · International Journal of Cardiology · doi:10.1016/j.ijcard.2014.10.152 · Cited by 27
Carvedilol Does not Alter the Insulin Sensitivity in Patients with Congestive Heart Failure
Refsgaard, J. C., Thomsen, C., Andreasen, F., & Gøtzsche, O. (2002) · European Journal of Heart Failure · doi:10.1016/s1388-9842(02)00035-1 · Cited by 27
Insulin Sensitivity in the Pathogenesis of Hypertension and Hypertensive Complications
Landsberg, L. (1996) · Clinical and Experimental Hypertension · doi:10.3109/10641969609088967 · Cited by 27
Beta-Blockers and Diabetes: The Bad Guys Come Good
Cruickshank, J. M. (2002) · Cardiovascular Drugs and Therapy · doi:10.1023/a:1022146721098 · Cited by 26
Carnevale, D. (2020) · Hypertension · doi:10.1161/hypertensionaha.120.14637 · Cited by 25
Insulin Resistance in Type 2 Diabetes
Yki‐Järvinen, H. (2010) · Wiley eBooks · doi:10.1002/9781444324808.ch11 · Cited by 27
Jung, J. Y., Oh, C., Ryoo, J., Choi, J., Choi, Y., Ham, W. T., & Park, S. K. (2018) · Endocrine · doi:10.1007/s12020-018-1530-7 · Cited by 26
Blockade of Angiotensin II Receptors Inhibits the Increase in Blood Pressure Induced by Insulin
Nakata, T., Takeda, K., Hatta, T., Kiyama, M., Moriguchi, J., Miki, S., Kawa, T., Morimoto, S., Nakamura, K., Uchida, A., et al. (1998) · Journal of Cardiovascular Pharmacology · doi:10.1097/00005344-199802000-00010 · Cited by 24
Wada, Y., Kidokoro, K., Kondo, M., Tokuyama, A., Kadoya, H., Nagasu, H., Kanda, E., Sasaki, T., Cherney, D. Z. I., & Kashihara, N. (2024) · Kidney International · doi:10.1016/j.kint.2024.05.006 · Cited by 23
Pioglitazone opposes neurogenic vascular dysfunction associated with chronic hyperinsulinaemia
Takatori, S., Zamami, Y., Yabumae, N., Hanafusa, N., Mio, M., Egawa, T., & Kawasaki, H. (2008) · British Journal of Pharmacology · doi:10.1038/bjp.2008.8 · Cited by 22
Masuo, K. (1996) · American Journal of Hypertension · doi:10.1016/0895-7061(96)00204-x · Cited by 22
Renal denervation in cardiometabolic disease: Concepts, achievements and perspectives
Grassi, G. M. (2012) · Nutrition Metabolism and Cardiovascular Diseases · doi:10.1016/j.numecd.2012.09.004 · Cited by 21
Hypertension and left ventricular hypertrophy in autosomal dominant polycystic kidney disease
Ecder, T., & Schrier, R. W. (2004) · Expert Review of Cardiovascular Therapy · doi:10.1586/14779072.2.3.369 · Cited by 21
Sympathetic neural activity, metabolic parameters and cardiorespiratory fitness in obese youths
Redón, P., Grassi, G. M., Redón, J., Álvarez‐Pitti, J., & Lurbe, E. (2016) · Journal of Hypertension · doi:10.1097/hjh.0000000000001200 · Cited by 20
NOMURA, M., Maruo, N., Zamami, Y., Takatori, S., Doi, S., & Kawasaki, H. (2007) · YAKUGAKU ZASSHI · doi:10.1248/yakushi.127.1877 · Cited by 20
Limberg, J. K., Smith, J. A. H., Soares, R. N., Harper, J. L., Houghton, K. N., Jacob, D. W., Mozer, M. T., Grunewald, Z. I., Johnson, B. D., Curry, T. B., et al. (2020) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00250.2020 · Cited by 20
Mori, K., Tanaka, M., Hosaka, I., Mikami, T., Endo, K., Hanawa, N., Ohnishi, H., & Furuhashi, M. (2023) · Hypertension Research · doi:10.1038/s41440-023-01179-0 · Cited by 19
Ali, M. Y., Jannat, S., & Chang, M. S. (2023) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.3c02115 · Cited by 18
Role of the arterial baroreflex in the sympathetic response to hyperinsulinemia in adult humans
McMillan, N. J., Soares, R. N., Harper, J. L., Shariffi, B., Moreno‐Cabañas, A., Curry, T. B., Manrique‐Acevedo, C., Padilla, J., & Limberg, J. K. (2022) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00391.2021 · Cited by 18
Selective alpha1-adrenoceptor blockade prevents fructose-induced hypertension
Tran, L. T., MacLeod, K. M., & McNeill, J. H. (2014) · Molecular and Cellular Biochemistry · doi:10.1007/s11010-014-2031-5 · Cited by 18
Do effects on blood pressure contribute to improved clinical outcomes with metformin?
Schäfers, R. F. (2003) · Diabetes & Metabolism · doi:10.1016/s1262-3636(03)72789-x · Cited by 18
Yao, Y., Wang, Q., Yang, J., Yan, Y., & Wei, W. (2024) · BMC Ophthalmology · doi:10.1186/s12886-024-03492-9 · Cited by 17
Jung, J. Y., Oh, C., Choi, J., Ryoo, J., & Park, S. K. (2018) · American Journal of Hypertension · doi:10.1093/ajh/hpy094 · Cited by 17
Nauck, M. A., Meier, J. J., Wolfersdorff, A. V., TILLIL, H., Creutzfeldt, W., & K�bberling, J. (2003) · Acta Diabetologica · doi:10.1007/s00592-003-0106-y · Cited by 17
Hyperinsulinemia blunts sympathetic vasoconstriction: a possible role of β-adrenergic activation
Limberg, J. K., Soares, R. N., Power, G. J., Harper, J. L., Smith, J. A. H., Shariffi, B., Jacob, D. W., Manrique‐Acevedo, C., & Padilla, J. (2021) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00018.2021 · Cited by 16
Wong, F. S.-H., Logan, A. G., & Blendis, L. M. (1996) · Hepatology · doi:10.1002/hep.510230304 · Cited by 16
Impaired response of cardiac autonomic nervous system to glucose load in severe obesity
Quilliot, D., Zannad, F. M., & Ziegler, O. (2005) · Metabolism · doi:10.1016/j.metabol.2005.03.002 · Cited by 16
Jemtel, T. H. L., Richardson, W., Samson, R., Jaiswal, A., & Oparil, S. (2017) · Current Hypertension Reports · doi:10.1007/s11906-017-0713-6 · Cited by 14
Takatori, S., Mizote, M., Zamami, Y., Kurosaki, Y., & Kawasaki, H. (2003) · British Journal of Pharmacology · doi:10.1038/sj.bjp.0705539 · Cited by 14
Haemodynamic actions of insulin
Tack, G. J. J., Lenders, J. W. M., Goldstein, D. S., Lutterman, J. A., Smits, P., & Thien, T. A. (1998) · Current Opinion in Nephrology & Hypertension · doi:10.1097/00041552-199801000-00016 · Cited by 14
Effects of Intra-Arterial Infusion of Insulin on Forearm Vasoreactivity in Hypertensive Humans.
Fujishima, S., Imaizumi, T., Abe, I., Takeshita, A., & Fujishima, M. (1995) · Hypertension Research · doi:10.1291/hypres.18.227 · Cited by 14
Muscle Sympathetic Nerve Activity in Patients with Acromegaly
Capaldo, B., Lembo, G., Rendina, V., Guida, R., Marzullo, P., Colao, A. A. L., Lombardi, G., & Saccà, L. (2000) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.85.9.6802 · Cited by 14
Self-citationTrovati, M., Massucco, P., Mattiello, L., Cavalot, F. L., Mularoni, E., Hahn, A., & Anfossi, G. (1996) · Diabetologia · doi:10.1007/bf02658501 · Cited by 14
Prevalence of hyperinsulinemia in young, nonobese Japanese men
Masuo, K., Mikami, H., Ogihara, T., & Tuck, M. L. (1997) · Journal of Hypertension · doi:10.1097/00004872-199715020-00006 · Cited by 13
Cardiovascular correlates of insulin resistance in normotensive and hypertensive African Americans
Kidambi, S., Kotchen, J. M., Krishnaswami, S., Grim, C. E., & Kotchen, T. A. (2010) · Metabolism · doi:10.1016/j.metabol.2010.07.036 · Cited by 13
Kopp, W. (2009) · The journal of nutrition health & aging · doi:10.1007/s12603-009-0005-1 · Cited by 13
Insulin and hypertension: Are they related?
Meehan, W. P., Darwin, C. H., Nb, M., Buchanan, T. A., & Saad, M. F. (1993) · Steroids · doi:10.1016/0039-128x(93)90105-v · Cited by 13
Scherrer, U. (1995) · Springer eBooks · doi:10.1007/978-3-642-79803-0_10 · Cited by 13
de la Fuente-Muñoz, M., Fernández, M. D. L. F., Roman, M. N., de la Cruz, M. D. C. I., Amor, S., Martorell, P., Enrique-López, M., Garcı́a-Villalón, Á. L., Inarejos-García, A. M., & Granado, M. (2022) · Antioxidants · doi:10.3390/antiox11081573 · Cited by 13
Paleczny, B., Siennicka, A. E., Zacharski, M., Jankowska, E. A., Ponikowska, B., & Ponikowski, P. P. (2016) · Clinical Autonomic Research · doi:10.1007/s10286-015-0338-2 · Cited by 12
The Interactions of the Immune System and the Brain in Hypertension
Perrotta, M., Lembo, G., & Carnevale, D. (2018) · Current Hypertension Reports · doi:10.1007/s11906-018-0808-8 · Cited by 13
Self-citationCao, L., Graham, S. L., & Pilowsky, P. M. (2018) · PLoS ONE · doi:10.1371/journal.pone.0198432 · Cited by 12
Zamami, Y., Fujiwara, H., 細田, 美., Hino, H., HIRAI, K., OKAMOTO, K., Jin, X. K., Takatori, S., Takai-Doi, S., & Kawasaki, H. (2010) · YAKUGAKU ZASSHI · doi:10.1248/yakushi.130.833 · Cited by 12
Insulin Resistance: Site of the Primary Defect or how the Current and the Emerging Therapies Work
Kolaczynski, J. W., & Caro, J. F. (1998) · Journal of Basic and Clinical Physiology and Pharmacology · doi:10.1515/jbcpp.1998.9.2-4.281 · Cited by 12
Effect of mild hyperisulinemia on conduit vessel endothelial function
Morgantini, C., Stea, F., Boldrini, B., Duranti, E., Ghiadoni, L., & Natali, A. (2012) · Journal of Hypertension · doi:10.1097/hjh.0b013e32834f9882 · Cited by 10
Insulin sensitivity in young women with vasovagal syncope
Ruiz, A., Calvar, C. E., Hermes, R., Rivadeneira, D., Bengolea, V., Chirife, R., TENTORI, M. C., & Gelpi, R. J. (2003) · American Heart Journal · doi:10.1016/s0002-8703(02)94707-1 · Cited by 11
I1 Agents: A New Approach to the Treatment of Hypertension
Dubar, M., & Pillion, G. (1995) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.1995.tb32459.x · Cited by 11
Tack, C. J., Heeremans, M., Thien, T. A., Lutterman, J. A., & Smits, P. (1996) · Journal of Cardiovascular Pharmacology · doi:10.1097/00005344-199608000-00010 · Cited by 11
Mozaffari, M. S., Roysommuti, S., & Wyss, J. M. (1996) · Journal of Cardiovascular Pharmacology · doi:10.1097/00005344-199604000-00013 · Cited by 11
Insulin-stimulated cardiac glucose uptake is impaired in spontaneously hypertensive rats
Morisco, C., Condorelli, G., Orzi, F., Vigliottá, G., Grezia, R. D., Bèguinot, F., Trimarco, B., & Lembo, G. (2000) · Journal of Hypertension · doi:10.1097/00004872-200018040-00017 · Cited by 11
Self-citationHalter, J. B. (1995) · Comprehensive physiology · doi:10.1002/cphy.cp110107 · Cited by 11
Lembo, M., Trimarco, V., Izzo, R., Pacella, D., Jankauskas, S. S., Gallo, P., Piccinocchi, R., Morisco, C., Piccinocchi, G., Bardi, L., et al. (2025) · Cardiovascular Diabetology · doi:10.1186/s12933-025-02798-2 · Cited by 11
Self-citationEffects of insulin on the cardiovascular integrating mechanisms of brain stem in cats
Kuo, S. W., Hsieh, J.-H., Wu, W., Horng, H. T., Shian, L. R., & Chai, C. Y. (1993) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.1993.265.4.e609 · Cited by 10
Funakoshi, S., Satoh, A., Maeda, T., Kawazoe, M., Ishida, S., Yoshimura, C., Tada, K., Takahashi, K., Ito, K., Yasuno, T., et al. (2021) · Hypertension Research · doi:10.1038/s41440-021-00727-w · Cited by 9
Elevated fasting serum insulin level predicts future development of hypertension
Park, S. K., Jung, J. Y., Choi, W. J., Kim, Y. H., Kim, H. S., Ham, W. T., Shin, H., & Ryoo, J. (2014) · International Journal of Cardiology · doi:10.1016/j.ijcard.2014.01.087 · Cited by 9
Cao, L., Graham, S. L., & Pilowsky, P. M. (2016) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00486.2015 · Cited by 9
The Role of the Autonomic Nervous System in Cardiovascular Toxicity
Carll, A. P., Farraj, A. K., & Roberts, A. M. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-801238-3.64259-9 · Cited by 9
Insulin Resistance and Blood Pressure
Ferrannini, E. (1999) · Humana Press eBooks · doi:10.1007/978-1-59259-716-1_15 · Cited by 10
Ciuceis, C. D., Rizzoni, D., Porteri, E., Boari, G. E. M., Zani, F., Miclini, M., Tiberio, G. A. M., Giulini, S. M., Paiardi, S., Rizzardi, N., et al. (2008) · Journal of Vascular Research · doi:10.1159/000128604 · Cited by 9
Physiologic hyperinsulinemia enhances counterregulatory hormone responses to hypoglycemia in IDDM.
Davis, M. R., Mellman, M., & Shamoon, H. (1993) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.76.5.8496333 · Cited by 32
Coexistence of hypertension with diabetes mellitus and its pharmacotherapy
Moke, E. G., Demaki, W. E., Daubry, T. M. E., Ataikiru, O., Agbonifo‐Chijiokwu, E., Ofulue, O. O., Ekuerhare, B. E., Akpoyovwere, O., Edje, K. E., & Isibor, N. P. (2023) · Scientia Africana · doi:10.4314/sa.v22i2.14 · Cited by 10
Genovesi, S., Montelisciani, L., Giussani, M., Lieti, G., Patti, I., Orlando, A., Antolini, L., & Parati, G. (2023) · Metabolites · doi:10.3390/metabo13030327 · Cited by 8
Insulin Resistance and Endothelial Dysfunction: Macro and Microangiopathy
Arce‐Esquivel, A. A., Aaron, K. E., Catherine, R., & Laughli, M. H. (2013) · InTech eBooks · doi:10.5772/56475 · Cited by 9
Dietary Sodium Restriction Impairs Endothelial Effect of Insulin
Vecchione, C., Morisco, C., Fratta, L., Argenziano, L., Trimarco, B., & Lembo, G. (1998) · Hypertension · doi:10.1161/01.hyp.31.6.1261 · Cited by 8
Self-citationTsuda, T., & Robinson, B. W. (2024) · Current Hypertension Reports · doi:10.1007/s11906-024-01313-4 · Cited by 7
Zhao, L., Zheng, L., Wang, R., Gong, X., Wu, Y., Han, S., Liu, L., & Xue, M. (2025) · Scientific Reports · doi:10.1038/s41598-025-93723-w · Cited by 7
Redón, P., Grassi, G. M., Redón, J., Álvarez‐Pitti, J., & Lurbe, E. (2019) · Blood Pressure · doi:10.1080/08037051.2019.1700777 · Cited by 7
Association between higher urinary normetanephrine and insulin resistance in a Japanese population
Murabayashi, M., Daimon, M., Murakami, H., Fujita, T., Sato, E., Tanabe, J., Matsuhashi, Y., Takayasu, S., Yanagimachi, M., Terui, K., et al. (2020) · PLoS ONE · doi:10.1371/journal.pone.0228787 · Cited by 7
Metwally, Y. G., Sedrak, H. K., & Shaltout, I. (2020) · The Egyptian Heart Journal · doi:10.1186/s43044-020-00099-5 · Cited by 7
The Adrenergic System in Cardiovascular Metabolism and Aging
Santulli, G. (2015) · Springer eBooks · doi:10.1007/978-3-319-13680-6_6 · Cited by 7
Klemenc, M., Maver, J., Princi, T., Flander, P., & Golja, P. (2008) · European Journal of Applied Physiology · doi:10.1007/s00421-008-0835-2 · Cited by 7
Failure of Acute Hyperinsulinemia to Alter Blood Pressure Is Not Due to Baroreceptor Feedback
Richey, J. S. (1999) · American Journal of Hypertension · doi:10.1016/s0895-7061(98)00272-6 · Cited by 7
Influence of nervous blockade on insulin-mediated glucose uptake in the human forearm
Lind, L., & Eriksson, M. B. (2003) · Metabolism · doi:10.1053/meta.2003.50069 · Cited by 6
Duanmu, Z., Scislo, T. J., & Dunbar, J. C. (1999) · Clinical and Experimental Hypertension · doi:10.3109/10641969909070847 · Cited by 6
Cardiovascular and sympathetic effects of reversing insulin resistance in hypertension
Grassi, G. M. (2004) · Journal of Hypertension · doi:10.1097/00004872-200409000-00007 · Cited by 6
Togane, Y. (1999) · Annals of Nuclear Medicine · doi:10.1007/bf03165423 · Cited by 5
Pharmacological approach to cardiovascular risk in metabolic syndrome
Bellis, A., & Trimarco, B. (2013) · Journal of Cardiovascular Medicine · doi:10.2459/jcm.0b013e32835dbd0d · Cited by 6
Self-citationEffect of renal denervation on glucose metabolism after a 12 month follow-up
Matous, D., Jiravský, O., Nykl, I., & Branny, M. (2015) · Biomedical Papers · doi:10.5507/bp.2015.030 · Cited by 5
The Role of Insulin Resistance in Cardiorenal Metabolic Syndrome
Xiao, J., Song, W. L., Huang, Y., He, X., Weng, Y., & Yu, H. (2025) · Cardiology in Review · doi:10.1097/crd.0000000000001048 · Cited by 5
Sha, Y., Cai, Y., Zeng, Y., & Fu, J. (2025) · Medicine · doi:10.1097/md.0000000000041585 · Cited by 4
Natali, A., & Nesti, L. (2021) · Metabolism · doi:10.1016/j.metabol.2021.154891 · Cited by 4
Ichikawa, Y., Watanabe, Y., Irie, K., Yokomichi, H., Horikoshi, T., Yoshizaki, T., Deyama, J., Kuroki, K., Uematsu, M., Kobayashi, T., et al. (2025) · Circulation Journal · doi:10.1253/circj.cj-24-0773 · Cited by 4
Imaizumi, T. (1996) · Hypertension Research · doi:10.1291/hypres.19.supplementi_s47 · Cited by 4
Lifestyle-Related Diseases and Metabolic Syndrome
Shiomi, N. (2022) · IntechOpen eBooks · doi:10.5772/intechopen.100992 · Cited by 4
Hypertension and Insulin Resistance
Natali, A., Taddei, S., & Ferrannini, E. (1997) · Humana Press eBooks · doi:10.1007/978-1-4757-3906-0_16 · Cited by 4
Insulin Response Patterns Contribute to Different Perinatal Risks in Gestational Diabetes
Yamada, H., Kato, E. H., 敦賀, 律., Yasuhiko, E., Kobashi, G., Sagawa, T., Makita, Z., Koike, T., & Fujimoto, S. (2001) · Gynecologic and Obstetric Investigation · doi:10.1159/000052903 · Cited by 4
Schwab, M., Bloch, J., Duplain, H., Sartori, C. S., & Scherrer, U. (2008) · PubMed · Cited by 2
Metadata
- Authors
- Lembo, G., Napoli, R., Capaldo, B., Rendina, V, Iaccarino, G., Volpe, M., Trimarco, B., & Saccà, L.
- Affiliations
- Federico II University Hospital (IT)
- Venue
- Journal of Clinical Investigation
- Published
- 1992-07-01
- Volume
- 90
- Issue
- 1
- Pages
- 24-29
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC443058
- OpenAlex
- W2159417090
- Semantic Scholar
- 8fe2d8db2d3c3ab4a67dd67a612135319f91815b
- Cited by
- 252
- References
- 47
- Citations by year
- 2026: 1 · 2025: 10 · 2024: 6 · 2023: 8 · 2022: 6 · 2021: 5 · 2020: 6 · 2019: 3 · 2018: 9 · 2017: 3 · 2016: 9 · 2015: 5 · 2014: 6 · 2013: 4 · 2012: 8
- FWCI
- 12.48
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Funders
- Società Italiana dell'Ipertensione Arteriosa
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
- Keywords
- essential hypertension, hyperinsulinemia, insulin resistance, skeletal muscle, sympathetic nervous system, noradrenaline release, glucose uptake
- MeSH terms
- Adult, Female, Humans, Hypertension, Insulin, Male, Muscles, Norepinephrine, Sympathetic Nervous System
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
