DOPAMINE IN THE CONSCIOUS DOG WITH CHRONIC HEART-BLOCK - MECHANISMS OF CHRONOTROPIC CARDIAC EFFECTS

The chronotropic effects of dopamine were studied in the conscious dog with chronic A-V block. Dopamine at 12.5-200 .mu.g/kg and 12.5-50 .mu.g/kg per min lowered atrial rate independently of dose. After blockade of muscarine receptors of .alpha.-adrenoceptors, it raised atrial rate. After blockade of dopamine receptors, dopamine still lowered atrial rate, and did so dose-relatedly after blockade of .beta.-adrenoceptors. It raised ventricular rate, and at high doses also induced ventricular rhythm disorders. Blockade of muscarine receptors enhanced the ventricular cardioaccelerator effect of dopamine (P < 0.025) at 100 .mu.g/kg, while blockade of .alpha.-adrenoceptors reduced it (P < 0.05). Blockade of dopamine receptors did not modify this effect, but blockade of .beta.-adrenoceptors reversed it. Dopamine at 25-200 .mu.g/kg raised mean blood pressure. This effect was enhanced by blockade of muscarine receptors, reversed by blockade of .alpha.-adrenoceptors, and was unaffected by blockade of .beta.-adrenoceptors or dopamine receptors. The atrial cardiomoderator effect of dopamine evidently is a vagal reflex response to its hypertensive action, and that it is limited by its direct .beta.-adrenergic stimulating action. The ventricular cardioaccelerator effect of dopamine apparently is attenuated by a reflex vagal depressor effect consequent to the induced hypertension. No evidence was found for the existence of positive chronotropic dopamine receptors in either atria or ventricles.