Biphasic neurogenic vasodilatation in the bovine intraocular long posterior ciliary artery: involvement of nitric oxide and an additional unidentified neurotransmitter.

We have investigated the neurogenic factors inducing relaxation in the intraocular segment of the bovine long posterior ciliary artery. In precontracted vessels, electrical field stimulation (EFS, 0.5-128 Hz, 10 s trains) in the presence of guanethidine (30 microM) evoked biphasic relaxation: optimal relaxation for the first and second components occurred at 10 and 50 s, respectively. The first component, but not the second, was abolished by L-NAME (100 microM) or ODQ (3 microM). Relaxation to exogenous CGRP (0.1-300 nM) was inhibited by the CGRP antagonist, CGRP(8-37) (1-5 microM), but neither component of neurogenic relaxation was affected. Preincubation with the sensory nerve excitotoxin, capsaicin (1 microM), had no effect on either the first or second components of neurogenic relaxation. Substance P (0.1 nM-0.1 microM) induced relaxation, but rapid and complete desensitisation occurred within minutes. Neither desensitisation to substance P (0.1 microM) nor incubation with the NK(1) antagonist, L-733,060 (0.3 microM), had any effect on the first or second components of neurogenic relaxation.VIP (0.1 nM-0.3 microM) induced relaxation and this was followed by substantial desensitisation. Neither desensitisation to VIP (0.6 microM) nor treatment with the protease, alpha-chymotrypsin (10 U ml(-1)), had any effect on the first or second components of neurogenic relaxation. The results indicate that nitric oxide mediates the first component of neurogenic relaxation in the bovine intraocular ciliary artery. The neurotransmitter mediating the second component remains to be determined but is unlikely to be CGRP, substance P or VIP.