Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.99.1 (NADPH-diaphorase)
 3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cellular localization patterns of NOS isoforms 1 and 3 (nNOS and eNOS, respectively) in the mammalian heart under basal (non-stimulated) working conditions are still a matter of discussion. Therefore, this issue was reinvestigated in rats using RT-PCR, Western blotting, catalytic histochemistry, immunohistochemistry and image analysis. Tongue and extensor digitorum longus muscles served as positive controls for NOS-1 and NOS-3. RT-PCR revealed NOS-1 mRNA and NOS-3 mRNA in atria and ventricles. Western blotting showed NOS-1 protein in atria and NOS-3 protein in the walls of both heart chambers. Localization of the activity of urea-resistant (and therefore specific) NADPH diaphorase (NADPH-D) and NOS-1 immunohistochemistry showed that NOS-1 is present in the sarcolemma region of a subpopulation of atrial cardiomyocytes but not in working and impulse-conducting cardiomyocytes of atria and ventricles. Atrial natriuretic peptide (ANP) immunohistochemistry revealed that a minority of the NOS-1-expressing atrial cardiomyocytes are myoendocrine cells. eNOS immunostaining was present in endothelial cells of capillaries of the conducting and working myocardium and endocardial cells. Image analysis of the activity of urea-resistant NOS diaphorase showed that NOS-1 activity is lower in the sarcolemma region of atrial cardiomyocytes than in that of tongue and extensor digitorum longus myofibers. These data suggest that, in the non-stimulated rat heart. NOS-1 is expressed in a subpopulation of atrial cardiomyocytes including myoendocrine cells, and that NOS-3 is expressed in the vascular and endocardial endothelium.
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PMID:Localization of NOS-1 in the sarcolemma region of a subpopulation of atrial cardiomyocytes including myoendocrine cells and NOS-3 in vascular and endocardial endothelial cells of the rat heart. 1266 87

Recently, we have shown that nitric oxide synthase-1 (NOS-1) and thus its product NO are present in the sarcolemma region of a subpopulation of atrial cardiomyocytes in the rat heart. In order to find out whether this newly discovered sarcolemma-associated NOS/NO system represents a general signalling mechanism in the murine rodent heart and whether its properties are comparable to those in skeletal muscle fibres, immunohistochemical and catalytic histochemical methods (including image analysis) were applied to the heart and extensor digitorum longus (EDL) and tongue muscles of wild type and mutant mice. In different strains of wild type mice and NOS-3 knockouts, urea-resistant (and therefore specific) NOS NADPH diaphorase histochemistry and NOS-1 immunohistochemistry revealed that NOS-1 activity and protein were present in the sarcolemma region of a subpopulation of atrial and ventricular working cardiomyocytes, but not in those of the impulse conducting system. Using image analysis, NOS-1 showed similar activities in the sarcolemma region of cardiomyocytes and in EDL type I myofibres. In mdx and NOS-1 knockout mice, NOS-1 was absent from the sarcolemma region of atrial and ventricular cardiomyocytes and of EDL and tongue muscle fibres, whereas NOS-1 was present in the hearts of NOS-3 knockouts. Atrial natriuretic peptide immunohistochemistry identified part of the atrial NOS-1-expressing cardiomyocytes as myoendocrine cells. In mdx mice as well as in NOS-1 - and NOS-3-deficient animals, the peptide was found in greater abundance than in wild type mice. These data suggest that NOS-1 is expressed in a subpopulation of working cardiomyocytes in the murine rodent heart, that the myoendocrine cells may be negatively modulated by NOS-1 - and NOS-3-produced NO, and that the anchoring mechanisms for NOS-1 in these cells (i.e. their confinement to the sarcolemma region) are comparable to those in skeletal muscle fibres.
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PMID:The nitric oxide synthase-1 and nitric oxide synthase-3/nitric oxide signalling systems in the heart of wild type mice and mouse mutants. 1276 67

Atrial natriuretic peptide (ANP) and nitric oxide (NO) induce diuresis, natriuresis and diminish vascular tone. Our previous studies showed NO system is involved in ANP hypotensive effect. The aim was to investigate ANP effects on renal and cardiac NO-synthase (NOS) activity. Rats were divided into two groups: group I, infused with saline (1 h, 0.05 ml/min); group II, received ANP bolus (5 microg/kg)+ANP infusion (1 h, 0.2 microg/kg x min). NADPH-diaphorase activity (NADPH-d) was determined in kidney and heart. NOS catalytic activity was determined in renal medulla and cortex and cardiac atria and ventricle by measuring the conversion of l-[U(14)C]-arginine to l-[U(14)C]-citrulline. In group I, NOS activity was determined in basal conditions and plus 1 microM ANP and in group II, NOS activity was determined in basal conditions. NADPH-d was higher in group II than in group I in glomeruli, proximal tubule, cortical and medullar collecting duct, right atria and left ventricle. NOS activity was increased by in vitro ANP addition and, in vivo, ANP infusion in all the studied tissues. ANP treatment increases renal and cardiac NO synthesis. This effect would be independent on the hemodynamic changes induced by ANP. The activation of NO pathway would be one of the mechanisms involved in diuretic, natriuretic and hypotensive effects of ANP.
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PMID:Atrial natriuretic peptide influence on nitric oxide system in kidney and heart. 1500 31