ArticleThe Histochemical journal
The nitric oxide synthase-1 and nitric oxide synthase-3/nitric oxide signalling systems in the heart of wild type mice and mouse mutants.
Article in The Histochemical journal. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 5 citations in OpenAlex.
- Nitric oxide control of cardiac function: is neuronal nitric oxide synthase a key component?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2004Review
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Authors and funding
3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
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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