Maintenance of baseline angiotensin II potentiates insulin-hypertension

H. L. Keen, Michael W Brands, E. W. Shek, J. E. Hall

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Chronic insulin infusion in rats increases mean arterial pressure (MAP) by a mechanism dependent on angiotensin II (AII). However, because plasma renin activity decreases with insulin infusion, this suggests that AII sensitivity is increased. Thus, the parallel reduction in AII may partly counteract any hypertensive action of insulin. This study tested the hypothesis that prevention of the insulin-induced fall in AII by clamping AII at baseline levels would potentiate insulin-hypertension. Sprague-Dawley rats were instrumented with artery and vein catheters, and MAP was measured 24 hrs/day. In 7 rats (A rats), renin-AII system activity was clamped at normal levels throughout the study by continuous infusion of an ACE inhibitor, benazepril, at 5 mg/kg/day i.v. (which by itself decreased MAP by 17±2 mmHg) together with AII at 5 ng/kg/min i.v.. Control MAP in the A rats averaged 99±1 mmHg. which was not different from the 101±2 mmHg measured before clamping AII levels; control MAP in the 8 vehicle rats averaged 105±2 mmHg. A 7 day infusion of insulin (1.5 mU/kg/min, i.v.) plus glucose (20 mg/kg/min, i.v.) increased MAP in both groups of rats; however, the increase in MAP was significantly greater in the A rats (12±1 vs. 5±1 mmHg). Thus, the chronic hypertensive action of insulin in rats is potentiated when AII levels are held constant at baseline levels and not allowed to fall.

Original languageEnglish (US)
JournalFASEB Journal
Issue number3
StatePublished - Dec 1 1997
Externally publishedYes

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics


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