Chronic intrarenal hyperinsulinemia does not cause hypertension

J. E. Hall, M. W. Brands, H. L. Mizelle, C. A. Gaillard, D. A. Hildebrandt

Research output: Contribution to journalArticle

64 Scopus citations

Abstract

Hyperinsulinemia has been postulated to link obesity and hypertension via the antinatriuretic actions of insulin. The main goal of this study was to quantitate the importance of the direct intrarenal actions of insulin, independent of systemic effects, in altering blood pressure and renal function. This was accomplished by determining the responses to chronic intrarenal insulin infusion in uninephrectomized, chronically instrumented conscious dogs maintained on a 74 meq/day sodium intake. Insulin was infused at rates calculated to raise intrarenal, but not systemic, insulin to levels similar to those observed in obese hypertensive dogs. Intrarenal insulin infusion (0.6 mU·kg-1·min-1) for 7 days caused transient decreases in sodium excretion but no significant changes in potassium excretion. Mean arterial pressure did not change during 7 days of insulin infusion, averaging 93 ± 4 mmHg during control and 93 ± 3 mmHg during insulin infusion. Intrarenal insulin caused small increases in GFR but no significant changes in effective renal plasma flow or renal vascular resistance. These results demonstrate that insulin causes transient decreases in sodium excretion, but chronic intrarenal hyperinsulinemia does not elevate blood pressure in normal dogs. Additional factors other than the direct sodium-retaining effects of insulin may be important in raising blood pressure in obesity-associated hypertension.

Original languageEnglish (US)
Pages (from-to)F663-F669
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume260
Issue number5 29-5
DOIs
StatePublished - 1991
Externally publishedYes

Keywords

  • Glomerular filtration rate
  • Kidney
  • Obesity
  • Sodium excretion

ASJC Scopus subject areas

  • Physiology

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