We investigated by immunocytochemistry (ICC) the acute effects of ischemia on the distribution in the rat heart of adrenomedullin (AM), a potent hypotensive peptide which is expressed in the cardiovascular system, where it is known to play a major regulatory and protective role. Hearts, collected from adult male Sprague-Dawley rats, were perfused with the Langendorff technique, and "global" ischemia was obtained by stopping perfusion for 20 min. Hearts were frozen, and ICC was performed using a specific anti-rat AM1-50 antibody and secondary peroxidase-conjugated antibodies. ICC demonstrated AM-immunoreactivity (IR) in cardiomyocytes and especially in the wall of coronary vessels. Quantitative densitometry showed that acute ischemia significantly decreased AM-IR in coronary arterioles, thereby suggesting that it markedly stimulates AM release. The conclusion is drawn that acute ischemia and ensuing hypoxia activate in the rat heart the release of AM, which by its coronarodilatory action may enhance heart blood flow.

Acute effect of ischemia on adrenomedullin immunoreactivity in the rat heart: An immunocytochemical study

BELLONI, ANNA SANDRA;GUIDOLIN, DIEGO;BOVA, SERGIO;
2004

Abstract

We investigated by immunocytochemistry (ICC) the acute effects of ischemia on the distribution in the rat heart of adrenomedullin (AM), a potent hypotensive peptide which is expressed in the cardiovascular system, where it is known to play a major regulatory and protective role. Hearts, collected from adult male Sprague-Dawley rats, were perfused with the Langendorff technique, and "global" ischemia was obtained by stopping perfusion for 20 min. Hearts were frozen, and ICC was performed using a specific anti-rat AM1-50 antibody and secondary peroxidase-conjugated antibodies. ICC demonstrated AM-immunoreactivity (IR) in cardiomyocytes and especially in the wall of coronary vessels. Quantitative densitometry showed that acute ischemia significantly decreased AM-IR in coronary arterioles, thereby suggesting that it markedly stimulates AM release. The conclusion is drawn that acute ischemia and ensuing hypoxia activate in the rat heart the release of AM, which by its coronarodilatory action may enhance heart blood flow.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11577/2474928
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