ABSTRACT
Vascular endothelium produces and releases a number of vasoactive substances with potent effects on vascular smooth muscle and circulating platelets. Some of these substances are potent vasodilators, others possess vasoconstrictor activity. Two such substances, en-dothelium-derived relaxing factor and the potent vasoconstrictor peptide endothelin may be considered potential, some would say real, chemical mediators in various shock states. The addition of nitric oxide, derived from the l-arginine pathway in a variety of cell types, to the long list of important chemical mediators in shock induced by endotoxin, stems from studies performed to elucidate the mechanisms of the loss of vascular reactivity that occur under these conditions and during sepsis. Vascular impairment can also be demonstrated in large blood vessels incubated in vitro with endotoxin or removed from animals to which endotoxin had been administered and then examined under in vitro conditions.
