AJP - Heart and Circulatory Physiology, Vol 272, Issue 4 1582-H1588, Copyright © 1997 by American Physiological Society
Nitric oxide-mediated neurogenic vasodilatation in isolated monkey lingual arteries
N. Toda, K. Ayajiki, M. Uchiyama and T. Okamura
Department of Pharmacology, Shiga University of Medical Sciences, Seta, Japan.
In isolated monkey lingual arteries denuded of the endothelium and
contracted with prostaglandin F2alpha, transmural electrical stimulation
produced a contraction that was reduced by prazosin and reversed to a
relaxation by additional treatment with alpha,beta-methylene ATP. The
relaxation thus induced was abolished by tetrodotoxin and
N(G)-nitro-L-arginine (L-NNA), a nitric oxide (NO) synthase inhibitor, and
L- but not D-arginine restored the response in the L-NNA-treated arteries.
Under treatment with prazosin and alpha,beta-methylene ATP, the arterial
strips responded to nicotine with a relaxation that was not influenced by
atropine and timolol but was abolished by hexamethonium, oxyhemoglobin, and
methylene blue. The nicotine-induced relaxation was abolished by L-NNA but
not by N(G)-nitro-D-arginine and was reversed by L-arginine. Relaxations to
exogenously applied NO (acidified NaNO2 solution) were not influenced by
L-NNA but were abolished by oxyhemoglobin and methylene blue. The response
was not affected in the strips made unresponsive to vasoactive intestinal
polypeptide and calcitonin gene-related peptide by desensitization.
Histochemical study demonstrated the presence of perivascular neurons
containing neuronal NO synthase. It is concluded that monkey lingual
arteries are innervated by vasoconstrictor nerves liberating norepinephrine
and possibly ATP and also by nonadrenergic noncholinergic vasodilator
nerves liberating NO as a neurotransmitter to activate soluble guanylate
cyclase. Vasoactive intestinal polypeptide and calcitonin gene-related
peptide do not appear to be involved in the neurogenic vasodilatation.
