IMR Press / FBE / Volume 2 / Issue 2 / DOI: 10.2741/E118

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.


Nitroxyl enhances myocyte Ca2+ transients by exclusively targeting SR Ca2+-cycling

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1 Department of Physiology & Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University, Columbus, OH 43210, USA
2 Cardiology Division, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
3 Department of Anesthesiology & Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, MD 21205, USA
4 Department of Clinical Medicine, Section of General Pathology, University of Perugia, Perugia, Italy

*Author to whom correspondence should be addressed.


Front. Biosci. (Elite Ed) 2010, 2(2), 614–626;
Published: 1 January 2010

Nitroxyl (HNO), the 1-electron reduction product of nitric oxide, improves myocardial contraction in normal and failing hearts. Here we test whether the HNO donor Angeli's salt (AS) will change myocyte action potential (AP) waveform by altering the L-type Ca2+ current (ICa) and contrast the contractile effects of HNO with that of the hydroxyl radical (.OH) and nitrite (NO2-), two potential breakdown products of AS. We confirmed the positive effect of AS/HNO on basal cardiomyocyte function, as opposed to the detrimental effect of .OH and the negligible effect of NO2-. Upon examination of the myocyte AP, we observed no change in resting membrane potential or AP duration to 20% repolarization with AS/HNO, whereas AP duration to 90% repolarization was slightly prolonged. However, perfusion with AS/HNO did not elicit a change in basal ICa, but did hasten ICa inactivation. Upon further examination of the SR, the AS/HNO-induced increase in cardiomyocyte Ca2+ transients was abolished with inhibition of SR Ca2+-cycling. Therefore, the HNO-induced increase in Ca2+ transients results exclusively from changes in SR Ca2+-cycling, and not from ICa.

Excitation-contraction coupling
L-type Ca2+ current
Action potential
Heart failure
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