Human uterine arterial relaxation induced by nitroxidergic nerve stimulation

N. Toda, T. Kimura, K. Yoshida, D. S. Bredt, S. H. Snyder, Y. Yoshida, T. Okamura

Research output: Contribution to journalArticlepeer-review

22 Scopus citations


Uterine arterial strips obtained from humans responded to nicotine with a contraction, which was abolished by prazosin. In the arteries treated with the α1-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 α1-adrenoceptors by neurogenic norepinephrine.

Original languageEnglish (US)
Pages (from-to)H1446-H1450
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number4 35-4
StatePublished - 1994
Externally publishedYes


  • immunohistochemistry
  • nitric oxide
  • nitric oxide synthase inhibitor
  • vasodilator innervation

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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