Mechanisms of the renal vasodilation caused by insulin in anesthetized pigs

Citation
C. Molinari et al., Mechanisms of the renal vasodilation caused by insulin in anesthetized pigs, LIFE SCI, 69(14), 2001, pp. 1699-1708
Citations number
22
Categorie Soggetti
Biochemistry & Biophysics
Journal title
LIFE SCIENCES
ISSN journal
00243205 → ACNP
Volume
69
Issue
14
Year of publication
2001
Pages
1699 - 1708
Database
ISI
SICI code
0024-3205(20010824)69:14<1699:MOTRVC>2.0.ZU;2-4
Abstract
The present study was planned to determine the mechanisms involved in the r enal vasodilation caused by insulin. Changes in flow caused by the intraven ous infusion of 0.004 IU/kg/min of insulin at constant heart rate, aortic b lood pressure, left ventricular contractility and blood levels of glucose a nd potassium in the left renal artery were assessed using an electromagneti c flowmeter. In ten pigs, infusion of insulin caused an increase in renal b lood flow which averaged 12.8% of the control values. After hemodynamic var iables had returned to control values, insulin infusion was repeated in fiv e pigs following blockade of a-adrenergic receptors with injection of phent olamine into the renal artery and in the other five pigs following blockade of nitric oxide formation with injection in the same artery of N-omega-nit ro-L-arginine methyl ester (L-NAME). After blockade of alpha -adrenergic re ceptors, insulin infusion caused an increase in renal blood flow which aver aged 12.8% of the control values, being significantly enhanced with respect to the increase previously obtained in the same pigs. On the contrary, aft er blockade of nitric oxide formation insulin infusion caused a decrease in renal blood flow which averaged 6.5% of the control values. These response s were respectively abolished by the subsequent injection into the: renal a rtery of L-NAME and phentolamine. The present study showed that the renal v asodilation caused by insulin in the anesthetized pig was the result of two opposite effects which involved a predominant vasodilation mediated by the release of nitric oxide from the endothelium and a sympathetic vasoconstri ctor mechanism mediated by alpha -adrenergic receptors. (C) 2001 Elsevier S cience Inc. All rights reserved.