Abstract
Abstract
In order to determine the possible etiology for diminished inotropic responsiveness to catecholamines in the infarction model of chronic congestive heart failure in rats, we studied β-adrenoceptor number and site-specific stimulated adenylate cyclase activity in noninfarcted left ventricular tissue of rats at 3 months after ligation of the left coronary artery. Rats were divided into sham, small infarct, and large infarct groups according to infarct size. The large infarct groups showed increased right ventricle to body weight ratio (0.93 ± 0.07 mg/g for the large infarcts vs 0.52 ± 0.02 and 0.54 ± 0.02 mg/g for the shams and small infarcts, respectively). β-Adrenoceptor number among the groups was similar (shams, 27 ± 1 fmol/mg; small infarcts, 26 ± 1 fmol/mg; and large infarcts, 29 ± 1 fmol/mg), as was Kd (20 ± 1 pmol, 18 ± 2 pmol, and 18 ± 2 pmol, respectively). Site-specific stimulation of adenylate cyclase using isoproterenol, Gpp(NH)p, forskolin, and MnCl2 revealed no significant differences among the groups. We conclude that this system is not responsible for the altered inotropic responsiveness to catecholamines seen in this model.
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