The mechanism underlying the vasodilator action of bunitrolol: contribution of alpha 1-adrenoceptor blocking action.

The mechanism of the vasodilator action of bunitrolol was investigated in pentobarbital-anesthetized dogs. When injected intraarterially, bunitrolol increased blood flow through the femoral arterial bed more effectively than that through the vascular bed of the left anterior descending coronary artery (LAD). The former is rich in alpha-adrenoceptors and tonically controlled by the sympathetic nerves, whereas the latter is not. Intraarterial prazosin increased femoral flow but not LAD flow, whereas intraarterial nitrendipine increased equieffectively both femoral and LAD flows. In the saphenous arterial bed of dogs that also underwent spinal anesthesia and received atropine and nadolol, intravenous bunitrolol suppressed more effectively vasoconstrictor responses to saphenous nerve stimulation than those to intraarterial norepinephrine. These effects of bunitrolol were similar to those of prazosin and dissimilar to those of yohimbine. In similarly treated dogs, bunitrolol suppressed more effectively increases in mean systemic arterial pressure in response to methoxamine than those to B-HT 920. From these results, it was concluded that an alpha 1-adrenoceptor blocking action is mainly involved in the acute vasodilator effect of bunitrolol. This action may also contribute to the decrease in total peripheral resistance seen in hypertensive patients treated chronically with bunitrolol.