Nitric Oxide

A specific difference-spectrophotometric method was used to measure nitric oxide (NO) release into the coronary effluent perfusate of isolated, constant-flow-perfused guinea pig hearts. Authentic NO applied into the coronary circulation decreased vascular resistance dose dependently and enhanced coronary release of cyclic GMP (cGMP) fivefold. Increasing oxygen tension in aqueous solutions from 150 to 700 mm Hg decreased NO half-life (5.6 seconds) by 32%. During single passage through the intact coronary system, 86% of the infused NO was converted to nitrite ions. Oxidation of NO was more than 30 times faster within the heart than in aqueous solution. Endogenously formed NO was constantly released into the coronary effluent perfusate at a rate of 161±+11 pmol/min. The NO scavenger oxyhemoglobin and methylene blue increased coronary resistance and decreased cGMP release (basal release, 342+±4 fmol/min), whereas superoxide dismutase reduced coronary resistance. L-Arginine (10` M) slightly decreased coronary perfusion pressure and enhanced release of cGMP. NG-Monomethyl L-arginine (10` M) reduced basal release of NO and cGMP by 26% and 31%, respectively, paralleled by a coronary vasoconstriction. Bradykinin in the physiological range from 5x 10`1 M to 10-7 M dilated coronary resistance vessels, which was paralleled by the release of NO and cGMP. Onset of NO release preceded onset of coronary vasodilation in all