HUMAN UTERINE ARTERIAL RELAXATION INDUCED BY NITROXIDERGIC NERVE-STIMULATION

Uterine arterial strips obtained from humans responded to nicotine with a contraction, which was abolished by prazosin. In the arteries treated with the al-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 N-G-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.