Nitric oxide synthase in cultured endocardial cells of the pig

Abstract

1 Endocardial cells release factors which regulate myocardial contractility and guanosine 3′:5′-cyclic monophosphate (cyclic GMP) levels. One of these factors is indistinguishable from endothelium-derived relaxing factor (EDRF). 2 The effluent from pig heart endocardial cells cultured on microcarrier beads caused the relaxation of a pig coronary artery ring denuded of endothelium. This relaxation was enhanced by a combination of superoxide dismutase and catalase and was attenuated by haemoglobin, which binds nitric oxide (NO), and by inhibitors of NO synthase, N^G-monomethyl-l-arginine (l-NMM A) or N^G-nitro-l-arginine. 3 A Ca²⁺-, l-arginine- and NADPH-dependent enzyme activity which generated NO was detected by a specific spectrophotometric assay in cytosol prepared from endocardial cells. The formation of NO was inhibited in a concentration-dependent manner by l-NMMA (but not d-NMMA) and this could be partially reversed upon addition of excess l-arginine. 4 Like endothelial cells from the blood vessels, the endocardial cells possess the ability to synthesize NO, which may act to regulate myocardial contractility.