Cyclic guanosine monophosphate mediates vascular relaxation induced by atrial natriuretic factor.

Abstract

The biochemical mechanism of action of synthetic atrial natriuretic factor (atriopeptin II) was studied in vascular smooth muscle of the rabbit thoracic aorta. Atriopeptin II caused a time-dependent and concentration-dependent increase in tissue levels of cyclic guanosine monophosphate that corresponded in these same tissues with vascular relaxation. The elevation of arterial cyclic guanosine monophosphate levels preceded the onset of vascular relaxation. Atriopeptin II did not alter vascular levels of cyclic adenosine monophosphate. The presence of a functionally intact vascular endothelium was not necessary for atriopeptin II to elicit vascular relaxation. Atriopeptin II-induced vascular relaxation and elevation of cyclic guanosine monophosphate levels were inhibited by the guanylate cyclase inhibitor methylene blue. These data suggest cyclic guanosine monophosphate mediates vascular relaxation produced by atriopeptin II.