Obesity and hypertension: Roles of hyperinsulinemia, sympathetic nervous system and intrarenal mechanisms

Michael W Brands, J. E. Hall, B. N. Van Vliet, M. Alonso-Galicia, G. A. Herrera, D. Zappe

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Hypertension is a well-recognized complication of obesity. However, the mechanisms for the development of obesity hypertension are not known. One mechanism proposed is that the hyperinsulinemia present in obese hypertensive patients causes hypertension via sodium retaining and/or sympathetic nervous system stimulatory effects. However, numerous studies in dogs have revealed no evidence for such chronic pressor actions of hyperinsulinemia. This is in close agreement with studies in human insulinoma patients that show marked hyperinsulinemia and normal blood pressure. The appropriateness of the dog as an experimental model is strengthened by reports from our laboratory and others that inducing obesity in dogs reproduces many of the characteristics of obesity in humans, including insulin resistance, hyperinsulinemia, sodium retention, hypertriglyceridemia and hypertension. Recent studies in obese dogs have indicated that significant increases in renal medullary cellularity and intercellular matrix deposition could contribute to the sodium retention and hypertension. Additional evidence suggests that sympathetic nervous system stimulation also may contribute to the elevated blood pressure. However, the mechanisms through which obesity induces these changes and the temporal relationship between these factors and the development of the hypertension remain to be determined.

Original languageEnglish (US)
JournalJournal of Nutrition
Volume125
Issue number6 SUPPL.
StatePublished - Jan 1 1995
Externally publishedYes

Fingerprint

Sympathetic Nervous System
Hyperinsulinism
Obesity
Hypertension
Dogs
Sodium
Blood Pressure
Insulinoma
Hypertriglyceridemia
Insulin Resistance
Theoretical Models
Kidney

Keywords

  • hypertension
  • insulin
  • kidney
  • obesity
  • sympathetic nervous system

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Nutrition and Dietetics

Cite this

Brands, M. W., Hall, J. E., Van Vliet, B. N., Alonso-Galicia, M., Herrera, G. A., & Zappe, D. (1995). Obesity and hypertension: Roles of hyperinsulinemia, sympathetic nervous system and intrarenal mechanisms. Journal of Nutrition, 125(6 SUPPL.).

Obesity and hypertension : Roles of hyperinsulinemia, sympathetic nervous system and intrarenal mechanisms. / Brands, Michael W; Hall, J. E.; Van Vliet, B. N.; Alonso-Galicia, M.; Herrera, G. A.; Zappe, D.

In: Journal of Nutrition, Vol. 125, No. 6 SUPPL., 01.01.1995.

Research output: Contribution to journalArticle

Brands, MW, Hall, JE, Van Vliet, BN, Alonso-Galicia, M, Herrera, GA & Zappe, D 1995, 'Obesity and hypertension: Roles of hyperinsulinemia, sympathetic nervous system and intrarenal mechanisms', Journal of Nutrition, vol. 125, no. 6 SUPPL..
Brands MW, Hall JE, Van Vliet BN, Alonso-Galicia M, Herrera GA, Zappe D. Obesity and hypertension: Roles of hyperinsulinemia, sympathetic nervous system and intrarenal mechanisms. Journal of Nutrition. 1995 Jan 1;125(6 SUPPL.).
Brands, Michael W ; Hall, J. E. ; Van Vliet, B. N. ; Alonso-Galicia, M. ; Herrera, G. A. ; Zappe, D. / Obesity and hypertension : Roles of hyperinsulinemia, sympathetic nervous system and intrarenal mechanisms. In: Journal of Nutrition. 1995 ; Vol. 125, No. 6 SUPPL.
@article{4c9ee6cd49f1461ca428d2bd0ac054de,
title = "Obesity and hypertension: Roles of hyperinsulinemia, sympathetic nervous system and intrarenal mechanisms",
abstract = "Hypertension is a well-recognized complication of obesity. However, the mechanisms for the development of obesity hypertension are not known. One mechanism proposed is that the hyperinsulinemia present in obese hypertensive patients causes hypertension via sodium retaining and/or sympathetic nervous system stimulatory effects. However, numerous studies in dogs have revealed no evidence for such chronic pressor actions of hyperinsulinemia. This is in close agreement with studies in human insulinoma patients that show marked hyperinsulinemia and normal blood pressure. The appropriateness of the dog as an experimental model is strengthened by reports from our laboratory and others that inducing obesity in dogs reproduces many of the characteristics of obesity in humans, including insulin resistance, hyperinsulinemia, sodium retention, hypertriglyceridemia and hypertension. Recent studies in obese dogs have indicated that significant increases in renal medullary cellularity and intercellular matrix deposition could contribute to the sodium retention and hypertension. Additional evidence suggests that sympathetic nervous system stimulation also may contribute to the elevated blood pressure. However, the mechanisms through which obesity induces these changes and the temporal relationship between these factors and the development of the hypertension remain to be determined.",
keywords = "hypertension, insulin, kidney, obesity, sympathetic nervous system",
author = "Brands, {Michael W} and Hall, {J. E.} and {Van Vliet}, {B. N.} and M. Alonso-Galicia and Herrera, {G. A.} and D. Zappe",
year = "1995",
month = "1",
day = "1",
language = "English (US)",
volume = "125",
journal = "Journal of Nutrition",
issn = "0022-3166",
publisher = "American Society for Nutrition",
number = "6 SUPPL.",

}

TY - JOUR

T1 - Obesity and hypertension

T2 - Roles of hyperinsulinemia, sympathetic nervous system and intrarenal mechanisms

AU - Brands, Michael W

AU - Hall, J. E.

AU - Van Vliet, B. N.

AU - Alonso-Galicia, M.

AU - Herrera, G. A.

AU - Zappe, D.

PY - 1995/1/1

Y1 - 1995/1/1

N2 - Hypertension is a well-recognized complication of obesity. However, the mechanisms for the development of obesity hypertension are not known. One mechanism proposed is that the hyperinsulinemia present in obese hypertensive patients causes hypertension via sodium retaining and/or sympathetic nervous system stimulatory effects. However, numerous studies in dogs have revealed no evidence for such chronic pressor actions of hyperinsulinemia. This is in close agreement with studies in human insulinoma patients that show marked hyperinsulinemia and normal blood pressure. The appropriateness of the dog as an experimental model is strengthened by reports from our laboratory and others that inducing obesity in dogs reproduces many of the characteristics of obesity in humans, including insulin resistance, hyperinsulinemia, sodium retention, hypertriglyceridemia and hypertension. Recent studies in obese dogs have indicated that significant increases in renal medullary cellularity and intercellular matrix deposition could contribute to the sodium retention and hypertension. Additional evidence suggests that sympathetic nervous system stimulation also may contribute to the elevated blood pressure. However, the mechanisms through which obesity induces these changes and the temporal relationship between these factors and the development of the hypertension remain to be determined.

AB - Hypertension is a well-recognized complication of obesity. However, the mechanisms for the development of obesity hypertension are not known. One mechanism proposed is that the hyperinsulinemia present in obese hypertensive patients causes hypertension via sodium retaining and/or sympathetic nervous system stimulatory effects. However, numerous studies in dogs have revealed no evidence for such chronic pressor actions of hyperinsulinemia. This is in close agreement with studies in human insulinoma patients that show marked hyperinsulinemia and normal blood pressure. The appropriateness of the dog as an experimental model is strengthened by reports from our laboratory and others that inducing obesity in dogs reproduces many of the characteristics of obesity in humans, including insulin resistance, hyperinsulinemia, sodium retention, hypertriglyceridemia and hypertension. Recent studies in obese dogs have indicated that significant increases in renal medullary cellularity and intercellular matrix deposition could contribute to the sodium retention and hypertension. Additional evidence suggests that sympathetic nervous system stimulation also may contribute to the elevated blood pressure. However, the mechanisms through which obesity induces these changes and the temporal relationship between these factors and the development of the hypertension remain to be determined.

KW - hypertension

KW - insulin

KW - kidney

KW - obesity

KW - sympathetic nervous system

UR - http://www.scopus.com/inward/record.url?scp=0029018312&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029018312&partnerID=8YFLogxK

M3 - Article

C2 - 7782935

AN - SCOPUS:0029018312

VL - 125

JO - Journal of Nutrition

JF - Journal of Nutrition

SN - 0022-3166

IS - 6 SUPPL.

ER -