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.