Cyclic guanosine monophosphate inhibition of contraction may be mediated through inhibition of phosphatidylinositol hydrolysis in rat aorta.

Abstract

The purpose of this study was to determine whether cyclic guanosine monophosphate inhibits contraction through inhibition of phosphatidylinositol hydrolysis. Sodium nitroprusside and atriopeptin II, agents which activate soluble and particulate guanylate cyclase, respectively, inhibited norepinephrine-induced contraction and accumulation of inositol monophosphate, a measure of phosphatidylinositol hydrolysis. Acetylcholine, an agent which elevates smooth muscle cyclic guanosine monophosphate levels through release of an endothelial-derived relaxing factor, induced similar inhibitory effects on contraction and inositol monophosphate accumulation in the presence but not absence of the endothelium. The cyclic nucleotide analogue 8-bromo cyclic guanosine monophosphate also inhibited contraction and inositol monophosphate accumulation. These results suggest that cyclic guanosine monophosphate may inhibit contraction through inhibition of phosphatidylinositol hydrolysis. Furthermore, the inhibition of phosphatidylinositol hydrolysis was independent of the mechanism by which cyclic guanosine monophosphate elevation occurred.