Insulin-induced hypertension in rats depends on an intact renin- angiotensin system

Michael W. Brands, David L. Harrison, Henry L. Keen, Angela Gardner, Eugene W. Shek, John E. Hall

Research output: Contribution to journalArticlepeer-review

60 Scopus citations

Abstract

This study tested the dependence of insulin-induced hypertension in rats on a functional renin-angiotensin system. Rats were instrumented with chronic artery and vein catheters and housed in metabolic cages. After acclimation, 10 rats began receiving the angiotensin-converting enzyme inhibitor (ACEI) benazepril at 1.8 mg · kg-1 · d-1 via a continuous intravenous infusion that was maintained throughout the study; 8 control rats received vehicle. Four days after starting ACEI or vehicle, all rats entered a 5-day control period that was followed by a 7-day insulin infusion at 1.5 mU · kg-1 · min-1. Glucose was coinfused at 22 mg · kg-1 · min-1 to prevent hypoglycemia. Insulin infusion in control rats increased mean arterial pressure (MAP; measured 24 h/d) from an average of 101±1 to 113±2 mm Hg on day 1; MAP averaged 110±1 mm Hg for the 7-day infusion period. Glomerular filtration rate decreased, although not significantly, from 2.7±0.1 to 2.1±0.2 mL/min on day 3. Chronic ACEI decreased baseline MAP from an average of 97±1 to 79±1 mm Hg and markedly attenuated the increase in MAP during insulin. MAP averaged 81±1 mm Hg for the 7-day period and increased significantly, to 85±2 mm Hg, only on day 3. Likewise, the tendency for glomerular filtration rate to decrease was blunted. These results indicate that insulin-induced hypertension in rats depends on angiotensin II and suggest that a reduction in glomerular filtration rate contributes to the shift in pressure natriuresis.

Original languageEnglish (US)
Pages (from-to)1014-1019
Number of pages6
JournalHypertension
Volume29
Issue number4
DOIs
StatePublished - Apr 1997
Externally publishedYes

Keywords

  • angiotensin II
  • blood pressure
  • glomerular filtration rate
  • insulin

ASJC Scopus subject areas

  • Internal Medicine

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