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Nitroxidergic nerve stimulation relaxes human uterine vein
1Department of Pharmacology, Shiga University of Medical Sciences, Seta, Japan.
Journal of the Autonomic Nervous System
|November 6, 1995
Summary
This study shows vasodilator nerves in human uterine veins release nitric oxide (NO) as a neurotransmitter. This NO helps regulate uterine vein tone, impacting blood flow.
Area of Science:
- Pharmacology
- Neuroscience
- Reproductive Biology
Background:
- Nitroglycerin, a nitric oxide (NO) donor, predominantly affects veins over arterioles.
- The role of endogenous NO from vasodilator nerves in regulating human uterine venous tone is not well understood.
Purpose of the Study:
- To investigate whether endogenous NO released from vasodilator nerves regulates the tone of human uterine venous strips.
- To identify the neurotransmitter responsible for vasodilation in human uterine veins.
Main Methods:
- Isolated human uterine venous strips were used.
- Vascular responses to nicotine were assessed in the presence of various antagonists, including prazosin (alpha 1-adrenoceptor antagonist), timolol, atropine, and indomethacin.
- The effects of oxyhemoglobin and NG-nitro-L-arginine (L-NA), a NO synthase inhibitor, on nicotine-induced relaxations were evaluated.
- Nitric oxide (NO)-induced relaxation was also studied in the presence of L-NA and oxyhemoglobin.
Main Results:
- Nicotine induced contractions or relaxations in partially contracted human uterine veins.
- Prazosin reversed nicotine-induced contractions to relaxations.
- Nicotine-induced relaxations in prazosin-treated strips were abolished by oxyhemoglobin and L-NA, but not by timolol, atropine, or indomethacin.
- L-NA's inhibitory effect was reversed by L-arginine, and its enantiomer D-NA was ineffective.
- NO-induced relaxation was unaffected by L-NA but abolished by oxyhemoglobin.
Conclusions:
- Human uterine veins are innervated by vasodilator nerves that liberate nitric oxide (NO) as a vasodilator neurotransmitter.
- Norepinephrine from adrenergic nerves contracts venous smooth muscle via alpha 1-adrenoceptor stimulation.