AJP - Heart and Circulatory Physiology, Vol 266, Issue 4 1446-H1450, Copyright © 1994 by American Physiological Society
Human uterine arterial relaxation induced by nitroxidergic nerve stimulation
N. Toda, T. Kimura, K. Yoshida, D. S. Bredt, S. H. Snyder, Y. Yoshida and T. Okamura
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
Uterine arterial strips obtained from humans responded to nicotine with a
contraction, which was abolished by prazosin. In the arteries treated with
the alpha 1-receptor antagonist and partially contracted with serotonin,
nicotine produced a relaxation that was not influenced by treatment with
atropine or timolol and endothelium denudation but was abolished by
hexamethonium, oxyhemoglobin, and NG-nitro-L-arginine (L-NNA). The
inhibitory effect of L-NNA was reversed by L- but not D-arginine.
Relaxations induced by nitroglycerin and nitric oxide (NO) were not
affected by L-NNA but were abolished by oxyhemoglobin. Transmural
electrical stimulation relaxed the arterial strips treated with prazosin;
this response was abolished by L-NNA and restored by L-arginine.
Histochemical study with NO synthase antiserum demonstrated the presence of
immunoreactive nerve fibers in the adventitia. It may be concluded that
human uterine arteries are innervated by vasodilator nerves that liberate
NO as a neurotransmitter after chemical or electrical stimulation.
Predominant vasoconstriction due to nerve stimulation appears to be
associated with activation of alpha 1-adrenoceptors by neurogenic
norepinephrine.
