Compelling clinical reports reveal that behavioral stress alone is sufficient to cause reversible myocardial dysfunction in selected individuals. We developed a rodent stress cardiomyopathy model by a combination of pre-natal and post-natal behavioral stresses (Stress). We previously reported a decrease in % FS by echo, both systolic and diastolic dysfunction by catheter-based hemodynamics, as well as attenuated hemodynamic and inotropic responses to the beta adrenergic agonist, isoproterenol (ISO) in Stress compared with matched Controls. We now report enhanced catecholamine responses to behavioral stress as evidenced by increased circulating plasma levels of norepinephrine (p<0.01) and epinephrine (p<0.01) in Stress vs Controls. Cardiac myocytes isolated from Stress also reveal evidence of oxidative stress as indicated by decreased ATP, increased GSSG and decreased GSH/GSSG ratio in the presence of increased glutathione peroxidase (GPX) and catalase activities (p<0.01, for each). We also report blunted inotropic and [Ca2+]i responses to extracellular Ca2+ ([Ca2+]out; p<0.05) as well as altered inotropic responses to the intracellular calcium regulator, caffeine (20mM; p<0.01). Treatment of cardiac myocytes with NAC (10-3 M) normalized calcium handling in response to ISO and [Ca2+]out and inotropic response to caffeine (p<0.01, for each). NAC also attenuated the blunted inotropic response to ISO and Ca2+ (p<0.01, for each). Surprisingly, NAC did not reverse the changes in GSH, GSSG or GSH/GSSG ratio. These data support a glutathione-independent salutary effect of NAC on intracellular calcium signaling in this rodent model of stress-induced cardiomyopathy.
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