Regulation of Vascular Homeostasis by Nitric Oxide

In 1980 Furchgott and Zawadzki (1) demonstrated that acetylcholine-induced relaxation of rings of rat thoracic aorta was dependent on the presence of an intact endothelium and was mediated by a labile humoral factor, which they later named endothelium-derived relaxing factor (EDRF). In 1987 it was shown that endothelial cells release nitric oxide gas (NO) in quantities sufficient to account for the vasodilator and platelet inhibitory effects of E D R F (2). Now, thirteen years later, NO has proven to be a widespread biological mediator playing roles in the most diverse biological functions including non-specific immunity reactions, neurotransmission in the central and peripheral nervous system, and modulation of hormone release (3). However. this chapter will be confined to reviewing the biological role of Ii0 in vascular hemostasis and the pathological changes that might occur in thrombotic vascular disease.

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