ROLE OF NO IN VASCULAR SMOOTH-MUSCLE AND CARDIAC-MUSCLE FUNCTION

NO is a key transducer of a vasodilator message from the endothelium t o vascular smooth muscle. Recently, its actions as a negative inotrope in cardiac muscle have been discovered. In the vasculature, it is syn thesized under physiological conditions following activation of a low- output, Ca2+-dependent NO synthase (NOS) in endothelial cells. Immune activation triggers the expression of a high-output, Ca2+-independent NOS in the vasculature and myocardium, causing the overproduction of N 0 and significant cardiovascular dysfunction. In this article, Richard Schulz and Chris Triggle briefly review recent findings concerning th e role of NO, and other endothelium-derived factors, in vascular smoot h muscle function and consider the consequences of its production in t he heart.