Effects of glucagon on adenyl cyclase activity in the left and right ventricles and liver in experimentally-produced isolated right ventricular failure

Abstract

We recently reported that glucagon neither augments right ventricular papillary muscle contractility nor increases adenyl cyclase activity in right ventricular particulate preparations in cats with chronic isolated right ventricular failure. To determine whether the defect in glucagon-mediated activation of adenyl cyclase was confined to the right ventricle, we studied the effects of glucagon on adenyl cyclase in particulate preparations of left ventricle and liver from cats in chronic right ventricular failure produced by pulmonary artery banding. In preparations from normal cats maximal increases in adenyl cyclase activity produced by glucagon averaged 57% in right ventricle, 80% in left ventricle and 500% in liver. Although glucagon concentration-response curves in particulate preparations from livers of normal and cats in chronic failure were identical, glucagon produced no significant changes in adenyl cyclase activity of the right ventricle or left ventricle from the cats with heart failure. Thus, the defect in adenyl cyclase responsiveness to glucagon caused by isolated right ventricular failure does not represent a generalized defect. The data do indicate, however, that isolated right ventricular failure leads not only to a decreased capacity of right ventricular adenyl cyclase to respond to glucagon stimulation, but also to a similar impairment of adenyl cyclase derived from the unstressed left ventricle.