Neurogenic vasoconstriction as affected by cholinergic and nitroxidergic nerves in dog ciliary and ophthalmic arteries.
OBJECTIVE
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, alpha,beta-methylene ATP, a P2alpha-purinoceptor antagonist, and BIBP3226, a neuropeptide Y receptor antagonist.


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 with alpha,beta-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 alpha,beta-methylene ATP. In the strips treated with L-NA, prazosin, and alpha,beta-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 stimulate alpha1-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.
Department of Pharmacology, Shiga University of Medical Science, Ohtsu, Japan.
M
M
Toda
T
T
Okamura
K
K
Ayajiki
N
N
Toda
D000109:Acetylcholine / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D001341:Autonomic Nervous System / Q000187:drug effects / Q000502:physiology*; D002799:Cholinergic Fibers / Q000502:physiology*; D019842:Ciliary Arteries / Q000294:innervation*; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D007537:Isometric Contraction / Q000187:drug effects; D008297:Male; D009131:Muscle, Smooth, Vascular; D009569:Nitric Oxide / Q000502:physiology*; D019335:Nitroarginine / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D009880:Ophthalmic Artery / Q000294:innervation*; D018340:Receptors, Adrenergic, alpha-1 / Q000378:metabolism*; D017476:Receptors, Neuropeptide Y / Q000037:antagonists & inhibitors; D018048:Receptors, Purinergic P2 / Q000378:metabolism*; D014661:Vasoconstriction / Q000502:physiology*
D000317:Adrenergic alpha-Antagonists; D018340:Receptors, Adrenergic, alpha-1; D017476:Receptors, Neuropeptide Y; D018048:Receptors, Purinergic P2; D019335:Nitroarginine; D009569:Nitric Oxide; D000255:Adenosine Triphosphate; D000109:Acetylcholine; C002630:alpha,beta-methyleneadenosine 5'-triphosphate; D009638:Norepinephrine