Intravenous injection of growth hormone in anaesthetized
pigs has been shown to cause coronary vasoconstriction by
antagonizing the vasodilatory effects of β2-adrenergic
receptors. Because nitric oxide is believed to modulate or
mediate β2-adrenergic effects, the present study was undertaken in the same
experimental model to determine the role of nitric oxide in the above
response to growth hormone. In fourteen pigs anaesthetized with sodium
pentobarbitone, changes in left circumflex or anterior descending coronary
blood flow caused by intravenous injection of 0.05 i.u. kg-1 of growth
hormone at constant heart rate and arterial blood pressure were assessed
using electromagnetic flowmeters. In a first control group of six pigs, growth
hormone caused a decrease in coronary blood flow which averaged 13.1 % of
the baseline values. In a second group of eight pigs, intravenous
administration of Nω-nitro-L-arginine methyl ester (L-NAME) was used to
block the endothelial release of nitric oxide. In these pigs, the subsequent
injection of growth hormone did not cause any significant changes in
coronary blood flow, even when performed after reversing the increase in
arterial blood pressure and coronary vascular resistance caused by L-NAME
with continuous intravenous infusion of papaverine. These results indicated
that the coronary vasoconstricting effect of growth hormone, known to
involve antagonism of β2-adrenergic vasodilatory effect, was mediated by
inhibition of nitric oxide release.