Systemic and Renal-Specific Sympathoinhibition in Obesity Hypertension
Open accessAbstract
Chronic pressure-mediated baroreflex activation suppresses renal sympathetic nerve activity. Recent observations indicate that chronic electric activation of the carotid baroreflex produces sustained reductions in global sympathetic activity and arterial pressure. Thus, we investigated the effects of global and renal specific suppression of sympathetic activity in dogs with sympathetically mediated, obesity-induced hypertension by comparing the cardiovascular, renal, and neurohormonal responses to chronic baroreflex activation and bilateral surgical renal denervation. After control measurements, the diet was supplemented with beef fat, whereas sodium intake was held constant. After 4 weeks on the high-fat diet, when body weight had increased ≈50%, fat intake was reduced to a level that maintained this body weight. This weight increase was associated with an increase in mean arterial pressure from 100±2 to 117±3 mm Hg and heart rate from 86±3 to 130±4 bpm. The hypertension was associated with a marked increase in cumulative sodium balance despite an approximately 35% increase in glomerular filtration rate. The importance of increased tubular reabsorption to sodium retention was further reflected by ≈35% decrease in fractional sodium excretion. Subsequently, both chronic baroreflex activation (7 days) and renal denervation decreased plasma renin activity and abolished the hypertension. However, baroreflex activation also suppressed systemic sympathetic activity and tachycardia and reduced glomerular hyperfiltration while increasing fractional sodium excretion. In contrast, glomerular filtration rate increased further after renal denervation. Thus, by improving autonomic control of cardiac function and diminishing glomerular hyperfiltration, suppression of global sympathetic activity by baroreflex activation may have beneficial effects in obesity beyond simply attenuating hypertension.
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Increased renal sympathetic nerve activity in individuals with obesity contributes to increases in renin secretion, sodium reabsorption and blood pressure.
“Increased RSNA in individuals with obesity contributes to increases in renin secretion, sodium reabsorption and BP159–161.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
The lack of effect of surgical renal denervation on plasma noradrenaline or heart rate suggests that sensory afferent signals from the kidneys to the brain may not make an important contribution to increases in sympathetic activity or cardiac autonomic dysfunction of obesity.
“In obese dogs, surgical RDN reduced renal tissue noradrenaline concentration by over 96% and almost completely abolished hypertension but did not lower plasma noradrenaline levels or HR, suggesting that sensory afferent signals from the kidneys to the brain may not make an important contribution to increases in sympathetic activity or cardiac autonomic dysfunction of obesity160.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
Renal denervation nearly normalized blood pressure in dogs with established obesity-induced hypertension.
“RDN also nearly normalized BP in dogs with established obesity-induced hypertension160,162 (FIG. 6).”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
Renal denervation did not restore baroreflex sensitivity despite abolishing obesity-induced hypertension in obese dogs.
“By contrast, RDN did not restore baroreflex sensitivity despite abolishing obesity-induced hypertension.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
In obese dogs, chronic baroreflex activation via electrical stimulation of the carotid sinuses reduced blood pressure, heart rate and heart rate variability and restored cardiac baroreflex sensitivity to control levels.
“In obese dogs, chronic baroreflex activation via electrical stimulation of the carotid sinuses reduced BP, HR and HR variability and restored cardiac baroreflex sensitivity to control levels160.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
In obese dogs, surgical renal denervation reduced renal tissue noradrenaline concentration by over 96% and almost completely abolished hypertension but did not lower plasma noradrenaline levels or heart rate.
“In obese dogs, surgical RDN reduced renal tissue noradrenaline concentration by over 96% and almost completely abolished hypertension but did not lower plasma noradrenaline levels or HR, suggesting that sensory afferent signals from the kidneys to the brain may not make an important contribution to increases in sympathetic activity or cardiac autonomic dysfunction of obesity160.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
Renal denervation did not decrease plasma noradrenaline concentration in obese dogs.
“Carotid sinus stimulation also decreased plasma noradrenaline concentration, suggesting global sympathoinhibition, whereas RDN did not have this effect.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
Baroreflex activation and renal denervation can abrogate renal sympathoexcitation.
“These observations highlight the importance of increased efferent RSNA in mediating obesity-induced hypertension and the capacity of baroreflex activation and RDN to abrogate renal sympathoexcitation160.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
Increased efferent renal sympathetic nerve activity is important in mediating obesity-induced hypertension.
“These observations highlight the importance of increased efferent RSNA in mediating obesity-induced hypertension and the capacity of baroreflex activation and RDN to abrogate renal sympathoexcitation160.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
Carotid sinus stimulation decreased plasma noradrenaline concentration in obese dogs.
“Carotid sinus stimulation also decreased plasma noradrenaline concentration, suggesting global sympathoinhibition, whereas RDN did not have this effect.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
Carotid sinus stimulation causes global sympathoinhibition.
“Carotid sinus stimulation also decreased plasma noradrenaline concentration, suggesting global sympathoinhibition, whereas RDN did not have this effect.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [160]
RDN also returned BP to nearly normal levels in established obesity hypertension in dogs.
“RDN also returned BP to nearly normal levels in established obesity hypertension in dogs68 (Figure 5).”
From Obesity-Induced Hypertension: Interaction of Neurohumoral and Renal Mechanisms (2015) · cites this paper as [68]
An implantable device for bilateral electric baroreceptor stimulation that decreases sympathetic tone alleviates obesity-associated hypertension in experimental and clinical settings.
“An implantable device for bilateral electric baroreceptor stimulation that decreases sympathetic tone alleviates obesity-associated hypertension in experimental and clinical settings (22–24).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [22]
Renal denervation did not lower the elevated heart rate or the plasma norepinephrine levels in the obese dogs.
“Interestingly, renal denervation did not lower the elevated heart rate or the plasma norepinephrine levels in the obese dogs (22).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [22]
Selective ablation of the renal nerves abolished hypertension in obese dogs independently from changes in body weight.
“Selective ablation of the renal nerves abolished the hypertension in obese dogs independently from changes in body weight (22).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [22]
Renal denervation in obese dogs led to a further increase in glomerular filtration rate whereas fractional sodium excretion remained suppressed.
“In fact, renal denervation in obese dogs led to a further increase in glomerular filtration rate whereas fractional sodium excretion remained suppressed (22).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [22]
Ablating the renal nerves in obesity reduced plasma renin activity presumably through inhibition of renal renin production and/or release.
“It should be noted, however, that ablating the renal nerves in obesity reduced plasma renin activity presumably through inhibition of renal renin production and/or release (22).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [22]
The sodium retention associated with experimental obesity appears due to an increase in tubular reabsorption of sodium as indicated by the increased glomerular filtration rate and decreased fractional sodium excretion.
“The sodium retention associated with experimental obesity appears due to an increase in tubular reabsorption of sodium as indicated by the increased glomerular filtration rate and decreased fractional sodium excretion (22).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [22]
Selective ablation of the renal nerves failed to correct the glomerular hyperfiltration observed in obesity.
“However, despite its efficacy to control blood pressure selective ablation of the renal nerves failed to correct the glomerular hyperfiltration observed in obesity (22).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [22]
Excessive sympathetic activity is a major cause of the abnormal sodium retention in obesity.
“Excessive sympathetic activity is a major cause of the abnormal sodium retention in obesity.”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [22]
Systemic sympathetic inhibition eliminated the renal abnormalities in obese dogs.
“This is supported by the finding that systemic sympathetic inhibition eliminated the renal abnormalities in obese dogs (22).”
From Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis (2014) · cites this paper as [22]
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- Authors
- Lohmeier, T. E., Iliescu, R., Liu, B., Henegar, J. R., Maric-Bilkan, C., & Irwin, E. D.
- Affiliations
- North Memorial Medical Center (US)
- From the Department of Physiology and Biophysics (T.E.L., R.I., B.L., C.M.-B.) and the Department of Pathology (J.R.H.), University of Mississippi Medical Center, Jackson, MS; Cardiovascular Research Department (R.I.), “Gr. T. Popa” Center for Biomedical Research, and the University of Medicine and Pharmacy, “Gr. T. Popa” Iasi, Romania; North Memorial Medical Center (E.D.I.), Trauma Services, Robbinsdale, MN.
- Venue
- Hypertension
- Published
- 2012-02
- Volume
- 59
- Issue
- 2
- Pages
- 331-338
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- PMC
- PMC3277854
- OpenAlex
- W2155568433
- Cited by
- 130
- References
- 50
- Citations by year
- 2025: 2 · 2024: 4 · 2023: 7 · 2022: 7 · 2021: 9 · 2020: 3 · 2019: 8 · 2018: 6 · 2017: 13 · 2016: 14 · 2015: 12 · 2014: 19 · 2013: 16 · 2012: 9
- FWCI
- 9.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL‐51971, P01HL051971)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Keywords
- obesity-related hypertension, renal denervation, renal sympathetic nerve activity, sympathetic nervous system, high-fat diet, sodium balance, fractional excretion of sodium, glomerular hyperfiltration, plasma renin activity, tachycardia
- MeSH terms
- Animals, Blood Pressure, Body Weight, Denervation, Disease Models, Animal, Dogs, Glomerular Filtration Rate, Hemodynamics, Hypertension, Kidney, Male, Obesity, Renin, Sympathetic Nervous System, Baroreflex, Diet, High-Fat
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.
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 ›
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