Regression of thyroid hormone induced cardiac hypertrophy: effect on cardiac beta receptors and adenyl cyclase activity.

摘要: Abstract Adrenergic mechanisms may be important in the symptomatic manifestations of hyperthyroidism. The chronic administration thyroid hormone also results cardiac hypertrophy and increased numbers beta-adrenergic receptors membranes. roles adrenergic initiation perpetuation this has been open to speculation. Rats treated chronically with L-thyroxin were sacrificed after 7 days treatment 1–4 cessation treatment. Hearts removed weighed norepinephrine measured. In other groups identically rats, membranes prepared from left ventricle for invitro measurements receptor characteristics adenyl cyclase activity. Regression a decrease number control values was seen as early 2 stopping thyroxine. Cardiac concentrations had returned at time. Displacement bound [H 3 ] dihydroalprenolol by isoproterenol not changed control. Basal stimulated activity thyroxine or its cessation. rapid reversal raises possibility that play regulatory role function. Although enhancement myocardial contractility mediated through effect is independent catecholamine sensitive system.