© 1997 by European Society of Cardiology
Copyright © 1997, European Society of Cardiology
Prostaglandins and nitric oxide mediate insulin-induced vasodilation in the human forearm
Hypertension Research Unit, Department of Nephrology, University Hospital, PO Box 9600, 2300 RC Leiden, Netherlands
* Corresponding author. Tel. +31 71 5262218; Fax +31 71 5248118; E-mail: P.C.Chang@Nephrology.MedFac.LeidenUniv.nl
Objective: To determine the involvement of prostaglandins, nitric oxide, and beta-adrenoceptor activation in insulin-induced vasodilation in the human forearm. Methods: Fifteen normal subjects were studied. Insulin was administered into the brachial artery in the presence of saline, the cyclo-oxygenase inhibitor indomethacin (0.65 µg/kg/min), the inhibitor of nitric oxide synthase NG-monomethyl-L-arginine (L-NMMA, 30 µg/kg/min), or the non-selective beta-adrenoceptor blocker propranolol (0.2 µg/kg/min). Forearm vascular resistance (FVR) was derived from forearm blood flow and concomitantly measured intra-arterial blood pressure. Results: Insulin decreased FVR by 32±5% (P<0.01). Both indomethacin and L-NMMA inhibited insulin-induced vasodilation, while propranolol had no effect. Single infusion of indomethacin was without effect on vascular tone, while single infusion of L-NMMA increased FVR by 81±19% (P<0.01). Conclusions: Insulin has vasodilating properties in skeletal muscle vasculature that is mediated by increases in nitric oxide, that subsequently stimulates prostaglandin release. The latter appears to be a novel vascular action of insulin.
KEYWORDS Insulin; Vasodilation; Adrenergic receptors; Indomethacin; EDRF; Human; Diabetes
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