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Cited by 152Blood Pressure and Hypertension StudiesSodium Intake and HealthCardiovascular Function and Risk Factors

Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis

Open access
Rahmouni, Kamal·2014·Hypertension
DOI 10.1161/hypertensionaha.114.00920PMC PMC4184930
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AI snapshot

Written from the paper’s full text.

TL;DR

This review synthesizes recent progress on mechanisms linking obesity and hypertension, emphasizing sympathetic overactivity, brain melanocortin/leptin/insulin pathways, adipose tissue factors, renal sodium retention, and vascular alterations. It concludes that neurogenic mechanisms are central and that better therapies require dissociating energy homeostasis from blood pressure control.

Key findings

  • Obesity-associated hypertension involves excessive sympathetic nerve activity: high-fat feeding in rabbits rapidly elevated renal sympathetic tone, blood pressure, and heart rate and impaired baroreflex function as soon as 1 week after diet onset, sustained after 3 weeks; rats showed increased lumbar sympathetic activity across the entire 24-hour period, primarily via increased burst amplitude rather than burst frequency.
  • The brain melanocortin system is implicated: MC4R loss-of-function mutations protected patients from obesity-associated elevations in blood pressure, heart rate, and sympathetic tone, whereas MC4R stimulation caused dose-dependent blood pressure increases in healthy overweight or obese subjects; leptin’s intravenous bolus in young healthy man increased muscle sympathetic nerve activity for over 2 hours.
  • Adipose tissue contributes through paracrine/endocrine and afferent mechanisms: adipocyte-derived aldosterone and angiotensinogen are linked to vascular and blood pressure effects; adipose-specific angiotensinogen deletion protected mice from high-fat-diet hypertension without altering weight gain; leptin receptor antagonist injected into fat depots in obese rats rapidly decreased renal sympathetic activity and arterial pressure for about 15 minutes.
  • Renal and vascular mechanisms are involved: renal denervation abolished hypertension in obese dogs independently of body weight but did not correct glomerular hyperfiltration; in the blinded, sham-controlled SYMPLICITY HTN-3 trial, renal denervation’s blood pressure-lowering effect after 6 months was not significantly different from sham. Vascular alterations such as arterial stiffness and endothelial dysfunction can precede hypertension and be reversed by weight loss, but are not universally associated with obesity.

Methods

  • Narrative review; no primary experimental data are reported.
  • Synthesizes clinical, animal, and human studies on mechanisms of obesity-associated hypertension, including radiotelemetry, microneurography, renal denervation, genetic mouse models, and adipose tissue studies.
  • Main analysis is qualitative synthesis of selected literature rather than systematic review or meta-analysis.

Limitations

  • The paper states that many important issues remain unaddressed: studies must dissociate energy homeostasis from blood pressure and vasomotor sympathetic control; there are still no specific guidelines for treating hypertension in obesity; clinical trials are needed; and pharmacogenomics should be integrated into personalized treatment.
  • The paper notes inconsistencies in renal denervation efficacy between studies, including the disappointing SYMPLICITY HTN-3 results.
  • Evident from the text: as a narrative review, it lacks a systematic search strategy, explicit inclusion criteria, formal risk-of-bias assessment, and quantitative synthesis.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1161/hypertensionaha.114.00920

Cites

120 of 120 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 124 cited sources checked · 0 supported · 0 flagged

  • Premisecitation

    Rats fed high fat diet exhibit a rapid increase in radiotelemetric lumbar sympathetic activity which progresses with time, in parallel with hemodynamic and metabolic changes.

    “Rats fed high fat diet also exhibited a rapid increase in radiotelemetric lumbar sympathetic activity which progresses with time, in parallel with hemodynamic and metabolic changes (21).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [21] Muntzel MS Al-Naimi OA Barclay A Ajasin D Cafeteria diet increases fat mass and chronically elevates lumbar sympathetic nerve activity in rats Hypertension 2012 60 1498 1502 23090774 PMC3535318 source

      Not checked in the free run.

  • Premisecitation
    § Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis

    Treatment with β-blockers leads to metabolic complications including weight gain.

    “Given that excessive sympathetic activity is common in obesity, β-blockers appear as an obvious pharmacologic therapy to treat the hypertension associated with this condition, but treatment with β-blockers leads to metabolic complications including weight gain (16–18).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [16] Julius S Valentini M Palatini P Overweight and hypertension - A 2-way street? Hypertension 2000 35 807 813 10720599 source

      Not checked in the free run.

    • cites [17] Zhou X Ma L Habibi J Whaley-Connell A Hayden MR Tilmon RD Brown AN Kim JA Demarco VG Sowers JR Nebivolol improves diastolic dysfunction and myocardial remodeling through reductions in oxidative stress in the Zucker obese rat Hypertension 2010 55 880 888 20176997 PMC2841702 source

      Not checked in the free run.

    • cites [18] Jordan J Engeli S Boschmann M Weidinger G Luft FC Sharma AM Kreuzberg U Hemodynamic and metabolic responses to valsartan and atenolol in obese hypertensive patients J Hypertens 2005 23 2313 2318 16269974 source

      Not checked in the free run.

  • Premisecitation

    Sympathetic overdrive is closely related to subclinical cardiovascular and renal alterations that develop in obese subjects even in the absence of hypertension.

    “Interestingly, sympathetic overdrive was also found to be closely related to subclinical cardiovascular and renal alterations that develop in obese subjects even in the absence of hypertension (19).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [19] Lambert E Sari CI Dawood T Nguyen J McGrane M Eikelis N Chopra R Wong C Chatzivlastou K Head G Straznicky N Esler M Schlaich M Lambert G Sympathetic nervous system activity is associated with obesity-induced subclinical organ damage in young adults Hypertension 2010 56 351 358 20625075 source

      Not checked in the free run.

  • Premisecitation
    § Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis

    Obesity is a major risk factor for resistant hypertension, i.e. uncontrolled blood pressure despite being on three or more antihypertensive medications.

    “Moreover, obesity is a major risk factor for resistant hypertension, i.e. patients who have uncontrolled blood pressure despite being on three or more antihypertensive medications (7;8).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [7] Goodfriend TL Calhoun DA Resistant hypertension, obesity, sleep apnea, and aldosterone: theory and therapy Hypertension 2004 43 518 524 14732721 source

      Not checked in the free run.

    • cites [8] Persell SD Prevalence of resistant hypertension in the United States, 2003–2008 Hypertension 2011 57 1076 1080 21502568 source

      Not checked in the free run.

  • Premisecitation
    § Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis

    Weight loss has a beneficial effect on blood pressure control.

    “Clinical and animal studies have documented that weight gain can raise arterial pressure whereas weight loss has a beneficial effect on blood pressure control (9–11).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [9] De CC Porteri E Rizzoni D Corbellini C La BE Boari GE Pilu A Mittempergher F Di BE Casella C Nascimbeni R Rosei CA Ruggeri G Caimi L Rosei EA Effects of weight loss on structural and functional alterations of subcutaneous small arteries in obese patients Hypertension 2011 58 29 36 21555677 source

      Not checked in the free run.

    • cites [10] Haufe S Utz W Engeli S Kast P Bohnke J Pofahl M Traber J Haas V Hermsdorf M Mahler A Busjahn A Wiesner S Otto C Mehling H Luft FC Boschmann M Schulz-Menger J Jordan J Left ventricular mass and function with reduced-fat or reduced-carbohydrate hypocaloric diets in overweight and obese subjects Hypertension 2012 59 70 75 22068866 source

      Not checked in the free run.

    • cites [11] Weisbrod RM Shiang T Al SL Fry JL Bajpai S Reinhart-King CA Lob HE Santhanam L Mitchell G Cohen RA Seta F Arterial stiffening precedes systolic hypertension in diet-induced obesity Hypertension 2013 62 1105 1110 24060894 PMC3951434 source

      Not checked in the free run.

  • May combine two claims. 18
  • Classified as probably not a substantial claim. 1

  • May combine two claims.

    Premisecitation

    In rabbits, these changes appeared as soon as 1 week after starting the high fat diet and were sustained after 3 weeks.

    “Indeed, these changes appeared as soon a 1 week after starting the high fat diet and sustained after 3 weeks (20).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [20] Armitage JA Burke SL Prior LJ Barzel B Eikelis N Lim K Head GA Rapid onset of renal sympathetic nerve activation in rabbits fed a high-fat diet Hypertension 2012 60 163 171 22647890 source

      Not checked in the free run.

  • May combine two claims.

    Premisenone given

    Activation of the sympathetic nervous system is a common feature of obesity and is widely recognized as a major contributor to the development and maintenance of hypertension.

    “Activation of the sympathetic nervous system which is a common feature of obesity is widely recognized as a major contributor to the development and maintenance of hypertension.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation
    § Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis

    Weight loss through lifestyle modifications for obesity-associated hypertension is neither simple nor sustained and is also not consistently effective as antihypertensive therapy.

    “At first glance, this recommendation seems compelling, but evidence suggests that weight loss through lifestyle modifications for obesity-associated hypertension is neither simple nor sustained and is also not consistently effective as antihypertensive therapy (15).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [15] Mark AL Dietary therapy for obesity: An emperor with no clothes Hypertension 2008 51 1426 1433 18474832

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Rabbits fed a high fat diet develop a rapid elevation in renal sympathetic tone, blood pressure and heart rate and impairment in baroreflex function.

    “Rabbits instrumented for telemetric recording of renal sympathetic activity and hemodynamic measurements were found to develop a rapid elevation in renal sympathetic tone, blood pressure and heart rate and impairment in baroreflex function when fed a high fat diet (20).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [20] Armitage JA Burke SL Prior LJ Barzel B Eikelis N Lim K Head GA Rapid onset of renal sympathetic nerve activation in rabbits fed a high-fat diet Hypertension 2012 60 163 171 22647890 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation
    § Obesity-Associated Hypertension: Recent Progress in Deciphering the Pathogenesis

    Genetic variants may impact the sensitivity to weight loss as well as blood pressure response to weight change.

    “In this regard, accumulating evidence suggests that genetic variants may impact the sensitivity to weight loss as well as blood pressure response to weight change.”
    Quote in the paperSubstantial claim0 of 2 sources checked
    • cites [12] Zhang X Qi Q Liang J Hu FB Sacks FM Qi L Neuropeptide Y promoter polymorphism modifies effects of a weight-loss diet on 2-year changes of blood pressure: the preventing overweight using novel dietary strategies trial Hypertension 2012 60 1169 1175 22966009 PMC3869086

      Not checked in the free run.

    • cites [13] Kostis WJ Cabrera J Hooper WC Whelton PK Espeland MA Cosgrove NM Cheng JQ Deng Y De SC Pyle M Maruthur N Reyes I Anderson CA Liu J Kostis JB Relationships between selected gene polymorphisms and blood pressure sensitivity to weight loss in elderly persons with hypertension Hypertension 2013 61 857 863 23438931 PMC4636329

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    High fat feeding in rats increased lumbar sympathetic discharge during the entire 24-hour period, primarily caused by a rise in burst amplitude and not through changes in burst frequency.

    “Further analysis revealed that high fat feeding in rats increased lumbar sympathetic discharge during the entire 24-hour period and this increase was primarily caused by a rise in burst amplitude and not through changes in burst frequency (21), indicating an increasing number of recruited nerve fibers.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [21] Muntzel MS Al-Naimi OA Barclay A Ajasin D Cafeteria diet increases fat mass and chronically elevates lumbar sympathetic nerve activity in rats Hypertension 2012 60 1498 1502 23090774 PMC3535318

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The melanocortin system has a powerful influence on energy homeostasis and is critically involved in mediating the metabolic, sympathetic and cardiovascular effects of leptin and insulin.

    “The melanocortin system has a powerful influence on energy homeostasis and is critically involved in mediating the metabolic, sympathetic and cardiovascular effects of leptin and insulin (32–35).”
    Quote in the paperSubstantial claim0 of 4 sources checked
    • cites [32] Hall JE da Silva AA do Carmo JM Dubinion J Hamza S Munusamy S Smith G Stec DE Obesity-induced Hypertension: Role of Sympathetic Nervous System, Leptin, and Melanocortins J Biol Chem 2010 285 17271 17276 20348094 PMC2878489 source

      Not checked in the free run.

    • cites [33] Harlan SM Rahmouni K Neuroanatomical determinants of the sympathetic nerve responses evoked by leptin Clin Auton Res 2013 23 1 7 22714900 PMC3496820

      Not checked in the free run.

    • cites [34] Carlson SH Wyss JM Mechanisms underlying hypertension and obesity: a melanocortin linkage in the brain Hypertension 2011 57 375 376 21263117

      Not checked in the free run.

    • cites [35] Ward KR Bardgett JF Wolfgang L Stocker SD Sympathetic response to insulin is mediated by melanocortin 3/4 receptors in the hypothalamic paraventricular nucleus Hypertension 2011 57 435 441 21263116 PMC3580160 source

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    Several brain nuclei are implicated in the renal sympathetic nerve activation triggered by leptin, consistent with the idea that leptin action in the brain involves a distributed network.

    “The fact that several brain nuclei are implicated in the renal sympathetic nerve activation triggered by leptin is consistent with the idea that leptin action in the brain involves a distributed network.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    Central administration of an insulin receptor antagonist to obese rabbits decreased arterial pressure, but with no concomitant change in renal sympathetic traffic.

    “Notably, central administration of an insulin receptor antagonist to obese rabbits also decreased arterial pressure, but with no concomitant change in renal sympathetic traffic (50).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [50] Lim K Burke SL Head GA Obesity-related hypertension and the role of insulin and leptin in high-fat-fed rabbits Hypertension 2013 61 628 634 23339171 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    The anti-contractile effects of perivascular adipose tissue extend to peripheral skeletal muscle arteries and involve the opening of a particular K+ channel (KCNQ) in smooth muscle.

    “The anti-contractile effects of perivascular adipose tissue has now been extended to peripheral skeletal muscle arteries and shown to involve the opening of a particular K+ channel (KCNQ) in smooth muscle (56).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [56] Zavaritskaya O Zhuravleva N Schleifenbaum J Gloe T Devermann L Kluge R Mladenov M Frey M Gagov H Fesus G Gollasch M Schubert R Role of KCNQ channels in skeletal muscle arteries and periadventitial vascular dysfunction Hypertension 2013 61 151 159 23184384

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    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).”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [22] Lohmeier TE Iliescu R Liu B Henegar JR Maric-Bilkan C Irwin ED Systemic and renal-specific sympathoinhibition in obesity hypertension Hypertension 2012 59 331 338 22184321 PMC3277854 source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    These mice had unaltered body weight, food intake and brown adipose tissue sympathetic responses to leptin.

    “However, these mice had unaltered body weight, food intake and brown adipose tissue sympathetic responses to leptin (42).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [42] Young CN Morgan DA Butler SD Mark AL Davisson RL The brain subfornical organ mediates leptin-induced increases in renal sympathetic activity but not its metabolic effects Hypertension 2013 61 737 744 23357182 PMC3832948

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    These vascular abnormalities are thought to contribute and even predict the development of hypertension and other cardiovascular complications.

    “These vascular abnormalities are thought to contribute and even predict the development of hypertension and other cardiovascular complications (9;11;64;69–71).”
    Quote in the paperSubstantial claim0 of 6 sources checked
    • cites [9] De CC Porteri E Rizzoni D Corbellini C La BE Boari GE Pilu A Mittempergher F Di BE Casella C Nascimbeni R Rosei CA Ruggeri G Caimi L Rosei EA Effects of weight loss on structural and functional alterations of subcutaneous small arteries in obese patients Hypertension 2011 58 29 36 21555677

      Not checked in the free run.

    • cites [11] Weisbrod RM Shiang T Al SL Fry JL Bajpai S Reinhart-King CA Lob HE Santhanam L Mitchell G Cohen RA Seta F Arterial stiffening precedes systolic hypertension in diet-induced obesity Hypertension 2013 62 1105 1110 24060894 PMC3951434

      Not checked in the free run.

    • cites [64] Belin de Chantemele EJ Ali MI Mintz JD Rainey WE Tremblay ML Fulton DJ Stepp DW Increasing peripheral insulin sensitivity by protein tyrosine phosphatase 1B deletion improves control of blood pressure in obesity Hypertension 2012 60 1273 1279 23045458 PMC3475734

      Not checked in the free run.

    • cites [69] Lurbe E Torro I Garcia-Vicent C Alvarez J Fernandez-Fornoso JA Redon J Blood pressure and obesity exert independent influences on pulse wave velocity in youth Hypertension 2012 60 550 555 22733475

      Not checked in the free run.

    • cites [70] Cao J Peterson SJ Sodhi K Vanella L Barbagallo I Rodella LF Schwartzman ML Abraham NG Kappas A Heme oxygenase gene targeting to adipocytes attenuates adiposity and vascular dysfunction in mice fed a high-fat diet Hypertension 2012 60 467 475 22753217 PMC3423899

      Not checked in the free run.

    • cites [71] Marshall NJ Liang L Bodkin J Dessapt-Baradez C Nandi M Collot-Teixeira S Smillie SJ Lalgi K Fernandes ES Gnudi L Brain SD A role for TRPV1 in influencing the onset of cardiovascular disease in obesity Hypertension 2013 61 246 252 23150506

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Improving insulin sensitivity in obese mice through Protein Tyrosine Phosphatase 1B deletion corrected the reduced albumin excretion, but not Na+ and K+ excretion nor the structural changes in the kidney.

    “For instance, improving insulin sensitivity in obese mice through Protein Tyrosine Phosphatase 1B deletion corrected the reduced albumin excretion, but not Na+ and K+ excretion nor the structural changes in the kidney (64).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [64] Belin de Chantemele EJ Ali MI Mintz JD Rainey WE Tremblay ML Fulton DJ Stepp DW Increasing peripheral insulin sensitivity by protein tyrosine phosphatase 1B deletion improves control of blood pressure in obesity Hypertension 2012 60 1273 1279 23045458 PMC3475734

      Not checked in the free run.

  • May combine two claims.

    Premisenone given

    Volume expansion and sodium retention are major features of obesity.

    “Volume expansion and sodium retention are major features of obesity.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Premisecitation

    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).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [22] Lohmeier TE Iliescu R Liu B Henegar JR Maric-Bilkan C Irwin ED Systemic and renal-specific sympathoinhibition in obesity hypertension Hypertension 2012 59 331 338 22184321 PMC3277854 source

      Not checked in the free run.

  • May combine two claims.

    Interpretationcitation

    Adipose tissue modulates blood pressure through its profound effect on Ang II synthesis, but the mechanisms involved remain to be defined.

    “Perhaps the most intriguing observation in this study relate to the demonstration that adipose tissue modulate blood pressure through its profound effect on Ang II synthesis, but the mechanisms involved remain to be defined (58).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [58] Grobe JL Rahmouni K The adipose/circulating renin-angiotensin system cross-talk enters a new dimension Hypertension 2012 60 1389 1390 23108659 PMC3959780

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Selective ablation of adipose tissue angiotensinogen did not alter the weight gain and other metabolic changes caused by high fat diet, but it protected mice from hypertension.

    “Selective ablation of adipose tissue angiotensinogen did not alter the weight gain and other metabolic changes caused by high fat diet, but it protected mice from hypertension (57).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [57] Yiannikouris F Gupte M Putnam K Thatcher S Charnigo R Rateri DL Daugherty A Cassis LA Adipocyte deficiency of angiotensinogen prevents obesity-induced hypertension in male mice Hypertension 2012 60 1524 1530 23108647 PMC3517298

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    Defects in various biological processes ranging from genetic and humoral factors to basic cellular signaling pathways in different tissues have been involved in the pathogenesis of obesity-related hypertension.

    “Defects in various biological processes ranging from genetic and humoral factors to basic cellular signaling pathways in different tissues have been involved in the pathogenesis of obesity-related hypertension.”
    Quote in the paperNot a substantial claim
    • Rests on an assumption: The obesity epidemic is associated with an increasing prevalence of cardiovascular risk factors including hypertension.
19 of 19

  • The paper relies on this without support.

    The obesity epidemic is associated with an increasing prevalence of cardiovascular risk factors including hypertension.

    “The epidemic of obesity is associated with raising prevalence of cardiovascular risk factors including hypertension.”

  • The paper relies on this without support.

    There are no specific guidelines for the treatment of hypertension in an obesity setting.

    “Also, despite the wide range of available anti-hypertensive drugs there are still no specific guidelines for the treatment of hypertension in an obesity setting.”
2 of 2

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?

  • Rodents with loss of function mutations in hypothalamic melanocortin-4 receptors are obese but lack sympathetic activation and obesity-associated hypertension.

    “Rodents with loss of function mutations in the hypothalamic melanocortin-4 receptors are obese but lack sympathetic activation and obesity-associated hypertension74,75.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [74]

  • The brain melanocortin pathway is crucial in the regulation of sympathetic activity and blood pressure in obesity.

    “The brain melanocortin pathway has emerged from studies in both experimental animals74,75 and humans89,90 as a crucial pathway in the regulation of sympathetic activity and BP in obesity.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [74]

  • Leptin contributes to sympathetic overactivity and hypertension in a number of animal models of monogenic and diet-induced obesity.

    “A large body of evidence has demonstrated that leptin contributes to sympathetic overactivity and hypertension in a number of animal models of monogenic and diet-induced obesity74–77.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [74]

  • Stimulation of hypothalamic melanocortin-4 receptors increases sympathetic activity and blood pressure.

    “In addition to inhibiting appetite and increasing metabolism, stimulation of hypothalamic melanocortin-4 receptors increases sympathetic activity and blood pressure74,75.”

    From The Sympathetic Nervous System Alterations in Human Hypertension (2015) · cites this paper as [74]

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.

  • Albumin excretion is described as both reduced and elevated

    Minor

    The paper says the obesity-related change corrected by treatment was reduced albumin excretion, but then describes that change as albuminuria, which denotes abnormally elevated urinary albumin excretion.

1 of 1

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Related

Authors
Rahmouni, K.
Affiliations
University of Iowa (US)
Corresponding author
Rahmouni, Kamal
ORCID
Rahmouni, Kamal
Venue
Hypertension
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2014-08
Volume
64
Issue
2
Pages
215-221
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
DOI
10.1161/hypertensionaha.114.00920
PMC
PMC4184930
OpenAlex
W2107915427
Cited by
150
References
120
Citations by year
2026: 4 · 2025: 6 · 2024: 6 · 2023: 7 · 2022: 2 · 2021: 9 · 2020: 9 · 2019: 12 · 2018: 13 · 2017: 19 · 2016: 16 · 2015: 20 · 2014: 2 · 2013: 2 · 2012: 3
FWCI
2.97
Type
journal article
Language
en
Open access
Locations
  • Hypertension (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Heart, Lung, and Blood Institute (HL-084207, P01HL084207)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Keywords
obesity, obesity-related hypertension
MeSH terms
Humans, Hypertension, Obesity

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