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Am J Physiol Cell Physiol 281: C342-C349, 2001;
0363-6143/01 $5.00
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Vol. 281, Issue 1, C342-C349, July 2001

Anti-adrenergic effects of nitric oxide donor SIN-1 in rat cardiac myocytes

Miroslav O. Stojanovic1, Mark T. Ziolo1,3, Gordon M. Wahler3, and Beata M. Wolska1,2

1 Department of Physiology and Biophysics, and 2 Section of Cardiology, Department of Medicine, College of Medicine, University of Illinois at Chicago, Chicago 60612; and 3 Department of Physiology, Midwestern University, Downers Grove, Illinois 60515

We studied how the nitric oxide (NO · ) donor 3-morpholinosydnonimine (SIN-1) alters the response to beta -adrenergic stimulation in cardiac rat myocytes. We found that SIN-1 decreases the positive inotropic effect of isoproterenol (Iso) and decreases the extent of both cell shortening and Ca2+ transient. These effects of SIN-1 were associated with an increased intracellular concentration of cGMP, a decreased intracellular concentration of cAMP, and a reduction in the levels of phosphorylation of phospholamban (PLB) and troponin I (TnI). The guanylyl cyclase inhibitor 1H-8-bromo-1,2,4-oxadiazolo (3,4-d)benz(b)(1,4)oxazin-1-one (ODQ) was not able to prevent the SIN-1-induced reduction of phosphorylation levels of PLB and TnI. However, the effects of SIN-1 were abolished in the presence of superoxide dismutase (SOD) or SOD and catalase. These data suggest that, in the presence of Iso, NO-related congeners, rather than NO · , are responsible for SIN-1 effects. Our results provide new insights into the mechanism by which SIN-1 alters the positive inotropic effects of beta -adrenergic stimulation.

3-morpholino-sydnonimine; phospholamban; troponin I; beta -adrenergic stimulation


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