Beta-Adrenoceptor Adenylate Cyclase System in Pig Myocardium with Stress Induced by Aortic Banding
Cardiac hypertrophy following pressure overload is generally considered a compensatory mechanism in the face of depressed mechanical performance of the myocardium. Although the underlying basis for the defective myocardial function is not well defined the contractile state of the myocardium is known to be influenced by a number of determinants and the most prominent among these determinants is the sympathetic activity. The inotropic influence of cardiac sympathetic activity is well established (1) and may play a significant role in supporting the heart under conditions of depressed state such as congestive heart failure. Various studies have demonstrated that the norepinephrine concentration in cardiac tissue is markedly reduced in patients with congestive heart failure (2). Similar reductions in cardiac norepinephrine concentrations have also been reported in experimentally induced right and left ventricular failure in animals (3,4). The cardiac muscle in hypertrophied heart has been reported to be more sensitive to the inotropic effects of catecholamines (5) and the depression in myocardial contractile function has been suggested to correlate roughly to the depletion in cardiac catecholamine stores (3,6). These observations suggest an altered interaction between the catecholamines and their membrane receptors in the hypertrophied heart.
KeywordsSucrose Filtration Depression EDTA Tyrosine
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