Dilation of isolated skeletal muscle arterioles by insulin is
endothelium-dependent and nitric oxide mediated.
Chen, Ya-Li, and Edward J. Messina.
Department of Physiology, New York Medical College, Valhalla, New
York 10595
APStracts 2:0522H, 1995.
Studies in humans and animals have shown that insulin administration
increases cardiac output and both forearm and hindlimb blood flow. In
this study we tested the hypothesis that insulin dilates skeletal
muscle arterioles and that the dilation is endothelium-dependent.
First order arterioles (77[mu]m) from rat cremaster muscle were
isolated, pressurized (65mmHg), equilibrated in a Krebs bicarbonate
buffered solution (pH 7.4) gassed with 10% O2 (5% CO2, 85% N2) and
studied in a no-flow state. Cumulative concentration-response curves
to insulin (10[mu]U-10mU/ml) were obtained in intact arterioles,
before and after either endothelium removal, indomethacin (IND, 10
-5M) or nitro-L-arginine (L-NNA, 10-4M). Insulin evoked concentration
-dependent increases in control diameter of 13-61%, that were
completely inhibited by endothelium removal or L-NNA. In contrast,
IND had no effect on insulin-evoked arteriolar dilation. These
results indicate that dilation to insulin in skeletal muscle
arterioles is endothelium-dependent and mediated by nitric oxide.
Received 13 July 1995; accepted in final form 9 November 1995.
APS Manuscript Number H648-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 December 95