Cardiovascular diseases and nitric oxide in humans.

The production of nitric oxide is impaired in patients with clinical and instrumental signs of arteriosclerosis (chronic coronary heart disease, stable and unstable angina, myocardial infarction); the NO deficiency is assessed through the vascular response to the infusion of stimulating (acetycholine) or inhibiting (N-mono-methylarginine) substances upon NO synthesis. Also in hypertensive subjects a weak endothelium-dependent vascular relaxation was documented, but this phenomenon is not constant and is still to be confirmed. In hypercholesterolemic patients a hyporesponsive endothelium-dependent vasodilation has been well documented, lipid lowering agents (drugs, apheresis) improve endothelium function. In heart failure low NO levels are found proportionally to the severity of disease: the expression of No is depressed, but cytokine mediated i NOS expression is enhanced, causing exaggerated amounts of NO and producing myocyte damage or death. Interesting findings indicated NO inhalation as a useful tool for reducing pulmonary hypertension and congestive heart failure.