Cardiac contractility, cAMP concentration, cAMP-dependent protein kinase, and phosphorylase activation during acute pressure overload.

The relationship between increases in myocardial contractility and cAMP and protein kinase activity were studied for hearts of normal rats and those with altered sympathectic capacity produced by the combined treatments of adrenalectomy, and 6-hydroxydopamine and propranolol injections. Increases in myocardial contractility, evaluated from intra-ventricular pressure changes, were produced by occlusion of the ascending aorta for 15, 20, or 25 s. Resting peak left ventricular pressure and the rate of rise of left ventricular pressure were lower (P less than 0.05) in sympathectomized animals, however, aortic occlusion abolished these differences. Time to peak tension and the relationship between end-diastolic pressure and developed pressure were unchanged by sympathectomy. ATP and CP concentrations in freeze clamped samples of the myocardium were lower (P less than 0.05) in both groups after aortic occlusion whereas lactate was elevated (P less than 0.05). Sympathectomy delayed and reduced the magnitude of the increase in the phosphorylase a/a + b ratio produced by aortic occlusion. Myocardial cAMP concentration was increased in the normal rats but decreased in sympathectomized animals after aortic occlusion. cAMP-dependent protein kinase activity followed the pattern of cAMP. The results demonstrate that heart possesses the capacity to increase its contractility to an acute, short-term overload even when devoid of sympathetic control.