Relaxant responses to transmural stimulation and nicotine of dog and monkey cerebral arteries

Abstract

In helical strips of dog and monkey [Macaca fuscata] cerebral arteries contracted with prostaglandin F2.alpha., transmural stimulation and nicotine produced relaxations abolished by tetrodotoxin and hexamethonium, respectively. These responses were attenuated by quinidine; relaxations of dog coronary arteries to transmural stimulation and isoproterenol were unaffected. Treatment with vasoactive intestinal polypeptide (VIP) and substance P (SP) abolished the relaxant response of cerebral arteries to repeated applications of VIP and SP, respectively; however, after VIP or SP, a normal relaxant response to transmural stimulation or nicotine was produced. Aminophylline suppressed relaxations induced by ATP but not by nerve stimulation. VIP, SP and ATP relaxed dog cerebral arteries; the responses were unaffected by quinidine. However, only VIP and ATP relaxed monkey cerebral arteries, and SP contracted the arteries. Acetylcholine contracted monkey arteries, in which transmural stimulation produced a relaxation. Nerves innervating the cerebroarterial wall are stimulated electrically and chemically by nicotine, resulting in the arterial relaxation. However, a vasodilator transmitter was not identified. Quinidine appears to selectively antagonize the action of the transmitter on cerebroarterial smooth muscle.