Abstract
NO has been shown to be a biologic substance important to normal physiologic functioning. It appears to be an endogenous vasodilator and is involved in hemostasis and inflammation. Endothelial cell dysfunction often leads to diminished NO production; this reduction in NO concentrations may be an etiologic factor in systemic hypertension, myocardial and splanchnic ischemia, atherosclerosis, CHF, and pulmonary vascular disease. A new class of drugs, NO donors, have potential utility in the treatment of coronary and pulmonary arterial diseases. Their major advantage over nitrates and nitroprusside is a lack of pharmacologic tolerance. Clinical trials with drugs of this class are now in progress.
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