Obesity, insulin resistance, and the renal circulation

John E. Hall, Michael W Brands, Eugene W. Shek, Jeffrey R. Henegar

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Weight gain causes high blood pressure in many essential hypertensive patients, and may be a major cause of ESRD. Although the precise mechanisms by which obesity raises blood pressure have not been fully elucidated, weight gain is associated with increased renal tubular reabsorption of sodium and a shift of pressure natriuresis toward higher blood pressures. The increased renal tubular reabsorption is compensated for, in part, by renal vasodilation and glomerular hyperfiltration. However, chronic renal vasodilation also raises hydrostatic pressure and wall stress in the glomeruli which, along with activation of neurohumoral factors and increased lipids and glucose intolerance, may cause glomerulosclerosis and loss of nephron function in obese subjects. The mechanisms by which obesity increases tubular reabsorption and shifts pressure natriuresis toward higher blood pressures are not completely understood, but do not appear to be directly related to hyperinsulinemia. Activation of the sympathetic and renin-angiotensin systems, as well as changes in intrarenal physical forces caused by medullary compression, appear to play a key role in the pathogenesis of obesity hypertension. However, the mechanisms that initiate these changes remain a fruitful area for further investigation, especially in view of the importance of weight gain as a cause of human essential hypertension and ESRD.

Original languageEnglish (US)
Title of host publicationAdvances in Organ Biology
Pages383-397
Number of pages15
StatePublished - Dec 1 2000

Publication series

NameAdvances in Organ Biology
Volume9
ISSN (Print)1569-2590

Fingerprint

Renal Circulation
Blood pressure
Insulin Resistance
Obesity
Insulin
Hypertension
Weight Gain
Natriuresis
Vasodilation
Chronic Kidney Failure
Chemical activation
Kidney
Pressure
Hydrostatic Pressure
Glucose Intolerance
Nephrons
Angiotensins
Hyperinsulinism
Hydrostatic pressure
Renin-Angiotensin System

ASJC Scopus subject areas

  • Biochemistry
  • Biochemistry, Genetics and Molecular Biology(all)
  • Obstetrics and Gynecology

Cite this

Hall, J. E., Brands, M. W., Shek, E. W., & Henegar, J. R. (2000). Obesity, insulin resistance, and the renal circulation. In Advances in Organ Biology (pp. 383-397). (Advances in Organ Biology; Vol. 9).

Obesity, insulin resistance, and the renal circulation. / Hall, John E.; Brands, Michael W; Shek, Eugene W.; Henegar, Jeffrey R.

Advances in Organ Biology. 2000. p. 383-397 (Advances in Organ Biology; Vol. 9).

Research output: Chapter in Book/Report/Conference proceedingChapter

Hall, JE, Brands, MW, Shek, EW & Henegar, JR 2000, Obesity, insulin resistance, and the renal circulation. in Advances in Organ Biology. Advances in Organ Biology, vol. 9, pp. 383-397.
Hall JE, Brands MW, Shek EW, Henegar JR. Obesity, insulin resistance, and the renal circulation. In Advances in Organ Biology. 2000. p. 383-397. (Advances in Organ Biology).
Hall, John E. ; Brands, Michael W ; Shek, Eugene W. ; Henegar, Jeffrey R. / Obesity, insulin resistance, and the renal circulation. Advances in Organ Biology. 2000. pp. 383-397 (Advances in Organ Biology).
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