Why the study?
Does myocyte-specific overexpression of eNOS alter myocardial contractile function and heart rate in mice?
Does myocyte-specific overexpression of eNOS alter myocardial contractile function and heart rate in mice?
High levels of endogenous myocyte-derived NO blunt myofilament calcium sensitivity and reduce basal contractility without altering intrinsic heart rate, suggesting NO is not a major modulator of neurohormonal control of myocardial function.
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Myocyte eNOS overexpression reduces contractility without altering heart rate in mice; leaves open NO's role in human myocardial calcium sensitivity.
Brünner et al. (2001) studied this question.
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