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

Circulatory Sciences Graduate Perfusion Program, Sarver Heart Center, University of Arizona, Tucson, Arizona

Tara Kelley

Circulatory Sciences Graduate Perfusion Program, Sarver Heart Center, University of Arizona, Tucson, Arizona

Douglas Larson

Circulatory Sciences Graduate Perfusion Program, Sarver Heart Center, University of Arizona, Tucson, Arizona

Vascular compliance is dependent on endogenous and exogenous sources of nitric oxide (NO). In a discussion of therapeutics and NO derived via nitric oxide synthase (NOS) enzymes, it is necessary to examine the pathways of each drug to provide the clinical perfusionist with a greater understanding of the role of NOS/NO in vascular function. Endothelial-derived NO is a contributor in the vasoregulation of vascular smooth muscle. Therapeutics seek to mimic the vasodilatory effects of the endogenous NO. The therapeutics included in this review are nitroglycerin, nitroprusside, amyl nitrite, and inhalation of NO. L-Arginine supplementation provides additional substrate for the endogenous pathway that can augment NO production. NO is a small bioactive molecule involved in various biochemical pathways. Dysregulation of NO production can impair normal physiologic control of vascular compliance. Therefore, the purpose of this review is to provide the perfusionist with an understanding of the biochemical and pharmacological aspects of NOS/NO associated with vascular function.

Perfusion, Vol. 15, No. 2, 97-104 (2000)
DOI: 10.1177/026765910001500203


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