Neurogenic vasoconstriction as affected by cholinergic and nitroxidergic nerves in dog ciliary and ophthalmic arteries

PURPOSE. To determine the involvement of noradrenergic and other vasoconstr ictor 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 th e canine posterior ciliary and external ophthalmic arteries denuded of the endothelium, which were stimulated by transmurally applied electrical pulse s (5 Hz). Vasoconstrictor mediators were analyzed by pharma cological antag onists, such as prazosin, alpha,beta-methylene ATP, a P-2X-purinoceptor ant agonist, 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 in hibitor. 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 physostigmin e and potentiated by atropine. Contractions induced by exogenous ATP were r eversed to relaxations by alpha,beta-methylene ATP. In the strips treated w ith L-NA, prazosin, and alpha,beta-methylene ATP, the addition of L-arginin e 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 stimulat ion are mediated by norepinephrine and ATP, which stimulate alpha(1)-adreno ceptor and P-2x purinoceptor, respectively. ATP from the nerve is unlikely involved in vasodilatation. Acetylcholine derived from the nerve impairs th e neurogenic contraction, possibly by interfering with the release of vasoc onstrictor transmitters, and neurogenic NO also inhibits the contraction po stjunctionally by physiological antagonism.