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