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Related Experiment Videos

Cholinergic nerve function in monkey ciliary arteries innervated by nitroxidergic nerve

N Toda1, M Toda, K Ayajiki

  • 1Department of Pharmacology, Shiga University of Medical Science, Ohtsu, Japan.

The American Journal of Physiology
|June 5, 1998
PubMed
Summary
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Neurogenic acetylcholine (ACh) contracts monkey ciliary arteries via muscarinic receptors. Vasodilation involves nitric oxide (NO) and is modulated by ACh interacting with nerve terminals.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Pharmacology

Background:

  • Ciliary arteries control ocular blood flow.
  • The role of neurogenic acetylcholine (ACh) in ciliary arterial tone is not fully understood.
  • Understanding these mechanisms is crucial for managing ocular conditions.

Purpose of the Study:

  • To investigate the control of ciliary arterial tone by neurogenic acetylcholine.
  • To elucidate the interplay between acetylcholine and vasodilator nerves.
  • To determine the specific receptors and pathways involved in ciliary artery regulation.

Main Methods:

  • Isolated posterior ciliary arteries from monkeys were used.
  • Acetylcholine and nicotine were applied in various concentrations.

Related Experiment Videos

  • Pharmacological agents like atropine, hexamethonium, and NG-nitro-L-arginine (L-NNA) were employed.
  • Transmural electrical stimulation was performed on arterial strips.
  • Histological examination identified nerve fibers and enzyme markers.
  • Main Results:

    • Acetylcholine induced dose-dependent contractions, independent of the endothelium, mediated by muscarinic receptors.
    • Vasodilation from nerve stimulation or nicotine involved nitric oxide (NO) synthesis from L-arginine.
    • Neurogenic ACh interfered with nitroxidergic nerve function via prejunctional muscarinic receptors.
    • High ACh concentrations stimulated nicotinic receptors, enhancing NO release.

    Conclusions:

    • Endogenous and exogenous ACh contracts monkey ciliary arteries via muscarinic receptors.
    • Nerve stimulation-induced vasodilation is mediated by NO synthesized from L-arginine.
    • Neurogenic ACh modulates nitroxidergic nerves, impacting ocular blood flow regulation.
    • ACh influences both vasoconstriction and vasodilation in ciliary arteries through distinct receptor pathways.