Paracrine and autocrine effects of nitric oxide on myocardial function.

摘要: Complex paracrine interactions exist between endothelial cells and cardiac myocytes in the heart. Cardiac release (or metabolize) several diffusible agents (e.g., nitric oxide [NO], endothelin-1, angiotensin II, adenylpurines) that exert direct effects on myocyte function, independent of changes coronary flow. Some these mediators are also generated by myocytes, often under pathological conditions. This review focuses role NO this paracrine/autocrine pathway. modulates aspects "physiological" myocardial function excitation-contraction coupling; relaxation; diastolic function; Frank-Starling response; heart rate; beta-adrenergic inotropic energetics substrate metabolism). The influenced its cellular enzymatic source, amount generated, presence reactive oxygen species, with neurohumoral other stimuli, relative activation cyclic GMP-dependent -independent signal transduction pathways. physiological importance endothelium- myocyte-derived remains to be established. In situations ischemia-reperfusion, left ventricular hypertrophy, failure, transplant vasculopathy rejection, myocarditis), can potentially beneficial or deleterious effects. Beneficial result from endothelial-type synthase-derived spatially temporally restricted expression inducible isoform, inducible-type synthase. Deleterious may (1) deficiency (2) excessive production, usually concurrent species production peroxynitrite formation. balance is key respect pathophysiological role.