Comparative pharmacology of nitric oxide and nitric oxide generators on cardiac contractility in mammalian species

Abstract

Nitric oxide (NO) is a potent vasorelaxing agent at nanomolar concentrations. At low nanomolar concentrations, NO also inhibits platelet aggregation, attenuates leukocyte adherence to the vascular endothelium, and quenches superoxide radicals. At high nanomolar concentrations, NO attenuates smooth muscle cells growth and stimulates proliferation of vascular endothelial cells. However, even at micromolar concentrations, NO fails to significantly alter cardiac contractility in isolated rat or cat cardiac muscle. Moreover, l-arginine, even at millimolar concentrations, fails to exert a decrease in cardiac contractility significantly greater than that produced by d-arginine.