Influence of hypothyroid status on dopamine-induced positive chronotropic and inotropic effects on isolated rat atria.

The involvement of alpha- and beta-adrenoceptors in dopamine (DA)-induced positive chronotropic and inotropic effects was investigated in isolated atria from euthyroid and hypothyroid rats. Propranolol at 3 x 10(-7) M remarkably inhibited the positive chronotropic effect of DA in both euthyroid and hypothyroid rats, and 1 x 10(-6) M phentolamine inhibited the effects of DA in the presence of propranolol in hypothyroid rats. Propranolol remarkably inhibited the positive inotropic effect of DA in both euthyroid and hypothyroid rats, while phentolamine was effective only in hypothyroid rats. In atria from reserpinized rats, the pD2-values for DA in both chronotropic and inotropic effects were reduced, but effectiveness of propranolol or phentolamine on DA-induced positive chronotropic and inotropic effects in euthyroid and hypothyroid rats was similar to that in non-reserpinized rats. In hypothyroid rats, DA increased the maximal rate of tension development, which was inhibited by both phentolamine and propranolol. DA shortened the duration of contraction. DA in the presence of phentolamine significantly shortened the duration of contraction but did not in the presence of propranolol. In conclusion the DA-induced positive chronotropic effect is mainly produced by beta-adrenoceptor stimulation in both euthyroid and hypothyroid rats, and also by a alpha-adrenoceptors to some extent in hypothyroid rats. The DA-induced positive inotropic effect is produced by alpha- as well as beta-adrenoceptor stimulation in both groups. However, alpha-adrenoceptors were involved to a greater extent in hypothyroid rats than in euthyroid rats. The stimulation of alpha-adrenoceptors by DA causes an increase in the maximal rate of tension development without a significant change in the duration of contraction, and the stimulation of beta-adrenoceptors by DA causes an increase in the maximal rate of tension development and shortening of the duration of contraction.