Purchase this article with an account.
Megumi Toda, Tomio Okamura, Kazuhide Ayajiki, Noboru Toda; Neurogenic Vasoconstriction as Affected by Cholinergic and Nitroxidergic Nerves in Dog Ciliary and Ophthalmic Arteries. Invest. Ophthalmol. Vis. Sci. 1999;40(8):1753-1760.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
purpose. To determine the involvement of noradrenergic and other vasoconstrictor
nerves in the contraction of ocular arteries and the modification by
cholinergic and nitroxidergic nerves of vasoconstrictor nerve function.
methods. Changes in isometric tension were recorded in helical strips of the
canine posterior ciliary and external ophthalmic arteries denuded of
the endothelium, which were stimulated by transmurally applied
electrical pulses (5 Hz). Vasoconstrictor mediators were analyzed by
pharmacological antagonists, such as prazosin, α,β-methylene ATP, a
P2X-purinoceptor antagonist, and BIBP3226, a neuropeptide Y
results. Transmural electrical stimulation produced contractions that were
potentiated by N G-nitro-l-arginine (L-NA), a
nitric oxide (NO) synthase inhibitor. The contraction was partially
inhibited by prazosin and abolished by combined treatment withα
,β-methylene ATP but was not influenced by BIBP3226.
Stimulation-induced contraction was attenuated by physostigmine and
potentiated by atropine. Contractions induced by exogenous ATP were
reversed to relaxations by α,β-methylene ATP. In the strips treated
with L-NA, prazosin, and α,β-methylene ATP, the addition of l-arginine elicited relaxations by nerve stimulation. The
ATP-induced relaxation was attenuated by aminophylline, whereas
neurogenic relaxation was unaffected.
conclusions. Ciliary and ophthalmic arterial contractions by nerve stimulation are
mediated by norepinephrine and ATP, which stimulateα 1-adrenoceptor and P2X purinoceptor,
respectively. ATP from the nerve is unlikely involved in
vasodilatation. Acetylcholine derived from the nerve impairs the
neurogenic contraction, possibly by interfering with the release of
vasoconstrictor transmitters, and neurogenic NO also inhibits the
contraction postjunctionally by physiological antagonism.
This PDF is available to Subscribers Only