PMID: 7546630Jun 1, 1995Paper

Endogenous nitric oxide in cardiovascular disease and transplantation

Annals of Medicine
G J Dusting, P S Macdonald

Abstract

Nitric oxide (NO), derived from the vascular endothelium and other cells of the cardiovascular system, has important roles in physiological regulation of blood flow and may have pathophysiological functions in cardiovascular disease. The mechanisms involved in NO-induced vasodilatation and cytotoxicity are briefly reviewed in the context of inflammatory reactions and cardiovascular function. Although NO can hyperpolarize vascular smooth muscle, activation of the endothelium can induce hyperpolarization and vasodilatation by other means. Endogenous inhibitors of NO generated by leucocytes may compromise blood flow distribution after ischaemia and reperfusion injury. Chronic heart failure is associated simultaneously with impairment of endothelium-dependent vasodilatation and with excess production of NO via the inducible NO synthase (iNOS), although it is unclear whether the latter ameliorates or exacerbates ventricular dysfunction. Excess NO production is also one of the earliest signs of transplant rejection, and suppression of iNOS expression by immunosuppressant drugs such as cyclosporin A might be one means by which these drugs protect allografts. Disturbances in the activity of NOS isoforms in the artery wall also accompan...Continue Reading

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Citations

Jan 16, 2007·Journal of Thrombosis and Thrombolysis·Luci Maria SantAna DusseBashir A Lwaleed
Feb 13, 2001·The Journal of Heart and Lung Transplantation : the Official Publication of the International Society for Heart Transplantation·D L LernerJ E Saffitz
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