Cardiovascular effects of bromocriptine in rats: role of peripheral adrenergic and dopaminergic receptors.

1. Experiments were designed to study the involvement of alpha-adrenoceptors and dopamine receptors in the hypotensive and bradycardic actions of bromocriptine in rats. 2. Intravenous administration of bromocriptine reduced blood pressure and heart rate which was inhibited by ganglionic blocking agents or by pithing. 3. The fall in blood pressure produced by bromocriptine was not modified by atropine, atenolol, prazosin, yohimbine, bilateral vagotomy or carotid ligation, but was blocked by sulpiride, domperidone and haloperidol. 4. The bradycardia produced by bromocriptine in intact rats was assumed to be mediated by the autonomic nervous system since it was partly reduced by bilateral vagotomy or atenolol, and entirely prevented by pithing. Furthermore, sulpiride but not yohimbine antagonized this effect. 5. In pithed rats, bromocriptine decreased both the pressor response (above 10 micrograms kg-1) and the tachycardia (above 50 micrograms kg-1) elicited by electrical stimulation of spinal cord outflow. Both effects were inhibited by sulpiride or yohimbine. 6. In pithed rats, bromocriptine did not affect the hypertension due to exogenous noradrenaline, phenylephrine, B-HT 920, nor the bradycardia evoked by stimulation of the cardiac muscarinic receptors by carbachol. 7. These results suggest that, in rats, bromocriptine produces hypotension via an action on presynaptic and/or ganglionic dopamine receptors, and causes bradycardia by activation of central dopamine receptors.