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Cited by 204Blood Pressure and Hypertension StudiesRenin-Angiotensin System StudiesRenal and Vascular Pathologies

Louis K. Dahl Memorial Lecture. Renal and cardiovascular mechanisms of hypertension in obesity.

Open access
Hall, J E·1994·Hypertension
DOI 10.1161/01.hyp.23.3.381
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Abstract

In all forms of hypertension, including human essential hypertension, pressure natriuresis is reset to higher blood pressures. Because human essential hypertension is a heterogeneous disease, it is likely that there are multiple neurohumoral and intrarenal causes of abnormal pressure natriuresis and increased blood pressure. Weight gain is recognized to be an important contributor to essential hypertension, although the mechanisms that link obesity with altered renal function and high blood pressure have not been fully elucidated. In obese dogs and humans, the shift of pressure natriuresis to higher blood pressures appears to be due mainly to increased tubular reabsorption, as glomerular filtration rate and renal plasma flow are increased compared with normal. Multiple causes of increased tubular reabsorption and hypertension in obesity have been postulated, including insulin resistance and hyperinsulinemia, activation of the sympathetic nervous and renin-angiotensin systems, and physical changes within the kidney itself. Support for the insulin resistance-hyperinsulinemia link between obesity and hypertension has been inferred mainly from acute and epidemiologic studies showing a correlation between insulin and blood pressure. Recent studies suggest that chronic hyperinsulinemia, comparable to that found in obesity, cannot account for obesity hypertension in dogs or humans. Activation of the sympathetic nervous system may play a role in obesity-induced hypertension, and there is evidence for a role of altered intrarenal physical forces caused by histological changes within the renal medulla. The quantitative importance of each of these abnormalities in altering renal function and raising blood pressure in obesity remains to be determined but is an important area of research for understanding human essential hypertension.

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  • In obese rabbits, dogs and humans, the levels of renal medullary glycosaminoglycans, especially hyaluronan, were markedly elevated compared with lean controls.

    “In obese rabbits, dogs and humans, the levels of renal medullary glycosaminoglycans, especially hyaluronan, which is an important component of the ECM and is often associated with tissue inflammation and oedema, were markedly elevated compared with lean controls53–55.”

    From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [53]

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Research works printed but not linked: 11

  1. Coleman TG. Blood Pressure Control, Volume I. St Albans, Vt: Eden Press Inc; 1980.
  2. DeWardener H. The primary role of the kidney in the aetiology of essential hypertension, Part 1. Clin Sci. 1990;79:193-200.
  3. Kawabe K, Watanbe TX, Shiono K, Solcabe H. Influences on blood pressure of renal isographs between spontaneously hyper- tensive and normotensive rats. Jpn Heart J. 1978;19:886-899.
  4. Rettig R, Stauss H, Folberth C, Gauten D, Waldherr R, Unger T. Hypertension transmitted from stroke-prone spontaneously hypertensive rats. Am J Physiol. 1989;257:F197-F203.
  5. Hall JE, Montani J-P, Woods LL, Mizelle H L Renal escape from vasopressin: role of pressure natriuresis. Am J Physiol. 1986;250: F907-F916.
  6. Chiang BW, Perlman LV, Epstein FH. Overweight and hyper- tension: a review. Circulation. 1969;39:403-421.
  7. Alexander J, Dustan HP, Sims EAH, Tarazi R. Report of the Hypertension Task Force, Volume 9. Washington, DC: US Gov- ernment Printing Office; 1979:61-77. US Dept of Health, Edu- cation, and Welfare publication 70-1631 (NIH).
  8. Hall JE, Herrera GA, Granger JP. Renal pathophysiology in obesity-induced hypertension. Hypertension. 1991;18:395. Abstract.
  9. Ferrari P, Weidmann P. Insulin, insulin sensitivity and hyper- tension. J Hypertens. 1990;8:491-500.
  10. Lucas CP, Estigarribia JA, Darga LL, Reaven GM. Insulin and blood pressure. Hypertension. 1985;7:702-706.
  11. Ferrannini E, Buzzigoli G, Bonadonna R, Giorico MA, Graziadel L, PedrineUi R, Brandi L, Bevilacqua S. Insulin resistance and hypertension. N EnglJ Med. 1987;317:350-357.

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Authors
Hall, J. E.
Affiliations
University of Mississippi Medical Center (US)
Corresponding author
Hall, J E
ORCID
Hall, J E
Venue
Hypertension
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1994-03
Volume
23
Issue
3
Pages
381-394
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
DOI
10.1161/01.hyp.23.3.381
OpenAlex
W2119269572
Cited by
204
References
111
Citations by year
2026: 1 · 2025: 1 · 2023: 2 · 2022: 2 · 2021: 2 · 2019: 5 · 2018: 6 · 2017: 1 · 2016: 5 · 2015: 5 · 2014: 8 · 2013: 6 · 2012: 3
FWCI
1.66
Type
journal article
Language
en
Open access
Locations
  • Hypertension (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01hl023502-13, 51971, 5p01hl011678-25)
  • National Heart, Lung, and Blood Institute (HL-23502, HL 11678, HL‐51971, P01HL051971)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Renal and Vascular Pathologies
Keywords
obesity-related hypertension, essential hypertension, pressure natriuresis, tubular sodium reabsorption, glomerular filtration rate, renal plasma flow, insulin resistance, hyperinsulinemia, sympathetic activation, renin-angiotensin system, renal medulla, renal function
MeSH terms
Animals, Humans, Hypertension, Insulin, Insulin Resistance, Kidney, Natriuresis, Obesity, Renin-Angiotensin System, Species Specificity, Sympathetic Nervous System, Weight Gain

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