The role of nitric oxide synthase/nitric oxide in vascular smooth muscle control

Vascular compliance is dependent on endogenous and exogenous sources of nit ric oxide (NO). In a discussion of therapeutics and NO derived via nitric o xide synthase (NOS) enzymes, it is necessary to examine the pathways of eac h drug to provide the clinical perfusionist with a greater understanding of the role of NOS/NO in vascular function. Endothelial-derived NO is a contr ibutor in the vasoregulation of vascular smooth muscle. Therapeutics seek t o mimic the vasodilatory effects of the endogenous NO. The therapeutics inc luded in this review are nitroglycerin, nitroprusside, amyl nitrite, and in halation of NO. L-Arginine supplementation provides additional substrate fo r the endogenous pathway that can augment NO production. NO is a small bioa ctive molecule involved in various biochemical pathways. Dysregulation of N O production can impair normal physiologic control of vascular compliance. Therefore, the purpose of this review is to provide the perfusionist with a n understanding of the biochemical and pharmacological aspects of NOS/NO as sociated with vascular function.