AJP - Heart and Circulatory Physiology, Vol 243, Issue 2 145-H153, Copyright © 1982 by American Physiological Society
Relaxant responses to transmural stimulation and nicotine of dog and monkey cerebral arteries
N. Toda
In helical strips of dog and monkey cerebral arteries contracted with
prostaglandin F2 alpha, transmural stimulation and nicotine produced
relaxations that were abolished by tetrodotoxin and hexamethonium,
respectively. These responses were attenuated by quinidine, whereas
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 adenosine
5'-triphosphate (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. It may be
concluded that nerves innervating the cerebrospinal 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 transmitters
on cerebroarterial smooth muscle.
