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Nitric oxide synthase in cultured endocardial cells of the pig
Author(s) -
Schulz R.,
Smith J.A.,
Lewis M.J.,
Moncada S.
Publication year - 1991
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1991.tb12378.x
Subject(s) - endothelium derived relaxing factor , nitric oxide , contractility , nitric oxide synthase , omega n methylarginine , chemistry , endothelium , cyclic guanosine monophosphate , arginine , guanosine , catalase , superoxide dismutase , biochemistry , medicine , enzyme , biology , endocrinology , amino acid
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 Ca 2+ ‐, 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.