Nitroxidergic nerve stimulation relaxes human uterine vein.

The predominant action of nitroglycerin, a nitric oxide (NO) donor, on veins over arterioles is well recognized. This study was carried out to determine whether endogenous NO derived from vasodilator nerve regulates the tone of human uterine venous strips. The isolated vein partially contracted with prostaglandin F2 alpha responded to nicotine with a contraction or a relaxation; the contraction was reversed to a relaxation by prazosin, and the relaxation was potentiated by the alpha 1-adrenoceptor antagonist. In prazosin-treated strips, nicotine-induced relaxations were not affected by timolol, atropine and indomethacin but were abolished by oxyhemoglobin and NG-nitro-L-arginine (L-NA), a NO synthase inhibitor. The D-enantiomer was without effect. The inhibition by L-NA was reversed by L-arginine. The NO-induced relaxation was not influenced by L-NA but was abolished by oxyhemoglobin. It may be concluded that the human uterine vein is innervated by vasodilator nerves from which NO is liberated as a vasodilator neurotransmitter. Norepinephrine from adrenergic nerves contracts venous smooth muscle possibly via stimulation of alpha 1-adrenoceptors.