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Nitric Oxide Synthase in Cultured Endocardial Cells of the Pig

Overview
Journal Br J Pharmacol
Publisher Wiley
Specialty Pharmacology
Date 1991 Sep 1
PMID 1723915
Citations 27
Authors
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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, NG-monomethyl-L-arginine (L-NMMA) or NG-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.

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References
1.
Martin W, Villani G, Jothianandan D, FURCHGOTT R . Selective blockade of endothelium-dependent and glyceryl trinitrate-induced relaxation by hemoglobin and by methylene blue in the rabbit aorta. J Pharmacol Exp Ther. 1985; 232(3):708-16. View

2.
Mulsch A, Bassenge E, Busse R . Nitric oxide synthesis in endothelial cytosol: evidence for a calcium-dependent and a calcium-independent mechanism. Naunyn Schmiedebergs Arch Pharmacol. 1989; 340(6 Pt 2):767-70. DOI: 10.1007/BF00169688. View

3.
Palacios M, Knowles R, Palmer R, Moncada S . Nitric oxide from L-arginine stimulates the soluble guanylate cyclase in adrenal glands. Biochem Biophys Res Commun. 1989; 165(2):802-9. DOI: 10.1016/s0006-291x(89)80037-3. View

4.
GIBSON Q, Roughton F . The kinetics and equilibria of the reactions of nitric oxide with sheep haemoglobin. J Physiol. 1957; 136(3):507-24. PMC: 1358871. DOI: 10.1113/jphysiol.1957.sp005777. View

5.
Lewis M, Shah A, Smith J, Henderson A . Does endocardium modulate myocardial contractile performance?. Cardioscience. 1990; 1(2):83-7. View