The Mechanism Underlying the Vasodilator Action of Bunitrolol: Contribution of α1-Adrenoceptor Blocking Action

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Abstract
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 was rich in .alpha.-adrenoceptors and tonically controlled by the sympathetic nerves, whereas the latter was 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, i.v. 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 [alefexole hydrochloride]. 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 seem in hypertensive patients treated chronically with bunitrolol.