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Pressor doses of angiotensin II increase hepatic glucose output and decrease insulin sensitivity in rats

R H Rao1

  • 1Department of Medicine, University of Pittsburgh School of Medicine, Philadelphia 15213, USA.

The Journal of Endocrinology
|February 1, 1996
PubMed
Summary
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Angiotensin II (AII) causes hypertension and hyperglycemia by increasing hepatic glucose output via a receptor-mediated pathway. This effect on glucose metabolism is independent of blood pressure changes.

Area of Science:

  • Endocrinology
  • Metabolic Physiology
  • Cardiovascular Research

Background:

  • The renin-angiotensin system plays a crucial role in blood pressure regulation.
  • The metabolic effects of angiotensin II (AII) are not fully understood, particularly in relation to glucose homeostasis.

Purpose of the Study:

  • To investigate the metabolic effects of angiotensin II (AII) on glucose metabolism under conditions of hyperinsulinemia.
  • To determine if the pressor effects of AII are linked to its metabolic actions on glucose.

Main Methods:

  • Utilized anesthetized rats under steady-state euglycemic hyperinsulinemia.
  • Administered varying doses of AII and measured hypertensive, hyperglycemic, hepatic glucose output (HGO), and glucose disposal.
  • Employed AII receptor antagonist saralasin to block AII effects.

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Main Results:

  • Pressor doses of AII (50 and 400 ng/kg/min) induced dose-dependent hypertension and hyperglycemia.
  • Both pressor doses of AII significantly increased hepatic glucose output (HGO) via a receptor-mediated mechanism.
  • Glucose disposal was significantly enhanced only at the lower pressor dose (50 ng/kg/min).
  • Saralasin blocked the metabolic effects of AII, indicating receptor mediation independent of blood pressure.

Conclusions:

  • Pressor doses of AII increase hepatic glucose output through a receptor-mediated mechanism unrelated to its pressor response.
  • The hyperglycemic effect of AII is partially counteracted by increased glucose disposal at lower doses.
  • Angiotensin II may play a role in in vivo glucose homeostasis, warranting further investigation.