Sensory neural mechanisms in contraction of the rabbit isolated sphincter pupillae: analysis of the responses to capsaicin and electrical field stimulation.

Electrical field stimulation produced contractions of the rabbit isolated iris sphincter muscle which were completely blocked by tetrodotoxin (10(-6) M). Low frequency (0.16-5 Hz) responses were atropine-resistant, but were prevented by sensory (trigeminal) denervation, and were considered to be owing to antidromic stimulation of sensory nerves. Higher frequency (10-40 Hz) responses were apparently unaffected by atropine alone (3 X 10(-7) M) and unaltered by sensory denervation, but were completely blocked by a combination of both. Thus at higher frequencies both cholinergic and sensory nerves would seem to be activated. Capsaicin-induced contraction of the isolated iris sphincter muscle, previously shown to be dependent upon an intact and functional sensory nerve supply, was not suppressed by atropine (3 X 10(-7) M) or by tetrodotoxin (10-6 M). Capsaicin therefore, although acting via sensory nerves, does not seem to require axonal conduction or Na+ flux to produce a response. This pain-producing substance may therefore act directly on sensory elements to release a mediator without requiring excitation of adjacent fibres by axon reflex. Contractile responses to capsaicin and also to low-frequency electrical stimulation were partially inhibited by morphine (5 X 10(-5) M), which in contrast had no effect on responses to carbachol or to substance P. Thus, at the peripheral as at the central endings of these bipolar primary afferent fibres, morphine may inhibit the release of the putative mediator.