We have recently established the distinct roles for endothelium-derived hyperpolarizing factor (EDHF) and NO in the bovine ocular vasculature (McNeish et al., 2001). In order to improve our understanding of this vascular bed, we wished to establish its neurogenic control. As a first approach, we sought to determine if, as previously reported (Wiencke et al., 1994), the intraocular long posterior ciliary artery (LPCA) was innervated by both nitrergic nerves and capsaicin-sensitive nerves that release CGRP.

Intraocular LPCA segments (430 ± 9 mm, internal diameter, n = 42) were dissected from bovine eyes obtained at a local abattoir. These were cut into 2 mm rings, mounted on a wire myograph and set to a transmural pressure equivalent of ~100 mmHg. Tissues were bathed in Krebs solution, gassed constantly with 95% O₂ / 5% CO₂ and maintained at 37^oC. Tone was induced using the thromboxane A 2-mimetic U46619 (0.1-1 µM). Nerves were stimulated by square wave pulses (10-18 V, 0.3 ms pulse width, 10 s train length, 0.5-128 Hz) from a Grass S88 stimulator. Adrenergic vasoconstriction was blocked using guanethidine (30 µM). Frequency response curves were obtained in the presence and absence of the NOS inhibitor L-NAME (100 µM), the neurotoxin tetrodotoxin (TTX, 0.1 µM), the sensory nerve excitotoxin capsaicin (1 µM) or the CGRP antagonist CGRP_8-37 (1 µM). Dilator responses are expressed as a percentage of active tone (assessed with papaverine, 500 µM). Data are expressed as mean ± SEM, with differences determined by ANOVA and the Bonferroni post test.

Responses to nerve stimulation were biphasic, comprising a rapid first component followed by a slower second component, peaking at 10 and 50 s, respectively (Table 1).

Table 1. First and second components of neurogenic relaxation at 32 Hz. * P<0.001, denotes a significant difference between control and treated vessels (n = 8-12). Negative values indicate reversal of relaxation to contraction.

Both components of vasodilatation are neurogenic since they were abolished by TTX. The first component only was also sensitive to L-NAME. However, neither component was affected by treatment with capsaicin or CGRP_8-37. Thus, although we agree that in the bovine intraocular LPCA the first component of neurogenic relaxation is nitrergic (Wiencke et al., 1994), we are unable to confirm that the second occurs via the release of CGRP from capsaicin-sensitive nerves. The identity of the transmitter responsible for the second component remains to be identified.

McNeish, A.J. et al. (2001). Br. J. Pharmacol., 134, 912-920
Wiencke, A.K. et al. (1994). Invest. Ophthalmol. Vis. Sci.35, 3268-3277