Triiodothyronine-induced changes in function, metabolism and weight of the rat heart: effects of alpha- and beta-adrenergic blockade.

The involvement of alpha- and beta-adrenergic receptors in the triiodothyronine (T3)-induced hemodynamic and metabolic alterations and in the development of cardiac hypertrophy was analyzed in time-course studies. Female Sprague-Dawley rats received daily injections of T3 (200 micrograms/kg s.c.) and a continuous i.v. infusion of 0.9% NaCl or alpha- or beta-receptor blocking agents. NaCl-injected animals served as controls. Eighteen hours after T3 administration, heart rate and LV dP/dtmax were considerably elevated. Cardiac output (CO) was not significantly changed. These alterations were abolished by simultaneous infusion of the beta-adrenergic blocker metoprolol. After 48 hours, CO as well as the cardiac RNA concentration were markedly elevated. The rise in LV dP/dtmax and heart rate was similar to the 18-h-value and was prevented by metoprolol. However, metoprolol did not influence the increase in CO and RNA concentration. Likewise, after 72 hours, metoprolol antagonized the T3-induced increase in heart rate and LV dP/dtmax, but had no effect on the elevation of CO and RNA concentration, the enhancement of adenine nucleotide synthesis and cardiac hypertrophy. Like metoprolol, the alpha-adrenergic blocker prazosin did not influence the T3-evoked cardiac hypertrophy. Thus, the development of cardiac hypertrophy in this model can occur independently of alpha- and beta-adrenergic stimulation.