Why the study?
Does short-term L-NAME treatment alter contractile function and Ca(2+) regulatory protein expression in left ventricular myocytes of Wistar rats?
Does short-term L-NAME treatment alter contractile function and Ca(2+) regulatory protein expression in left ventricular myocytes of Wistar rats?
Short-term NOS inhibition with L-NAME in rats improves cardiomyocyte contractile function and increases expression of Ca2+ regulatory proteins without altering in vivo hemodynamics.
Short-term L-NAME may enhance rat myocyte contractility without hemodynamic effects; leaves open translation to human cardiac therapy.
The main purpose of this study was to investigate the effects of short-term L-NAME treatment on the contractile function of left ventricle (LV) myocytes and the expression of proteins related to Ca(2+) homeostasis. Data from Wistar rats treated with L-NAME (L group, n = 20; 0.7 g/L in drinking water; 7 days) were compared with results from untreated controls (C group, n = 20). Cardiomyocytes from the L group showed increased (p < 0.05) fractional shortening (23%) and maximum rate of shortening (20%) compared with the C group. LV from the L group also showed increased (p < 0.05) expression of the ryanodine receptor 2 and Na(+)/Ca(2+) exchanger proteins (76% and 83%, respectively; p < 0.05). However, the L and C groups showed similar in vivo hemodynamic parameters of cardiac function. In conclusion, short-term NOS inhibition determines an increased expression of Ca(2+) regulatory proteins, which contributes to improving cardiomyocyte contractile function, preserving left ventricular function.
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Lunz et al. (2011) studied this question.
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