| Abstrakt: |
To find out whether, and which type of, adrenoceptors mediate prejunctional inhibition of sensory neurotransmitter release from trigeminal fibres, the modulation of twitch response to electrical field stimulation on rabbit isolated iris was investigated. Evoked iris sphincter contractions consisted of a minor fast cholinergic and a large slow component. The latter was unaffected by atropine and guanethidine, hence nonadrenergic noncholinergic in nature (NANC), but nearly completely abolished by capsaicin pretreatment and by the neurokinin receptor antagonist spantide. The response was probably not mediated by NK receptors as SR 48,968, an NK selective nonpeptide antagonist, failed to reduce the response to the release of the endogenous neurokinin(s) (and exogenous substance P), but in part due to NK receptor activation as shown by a reduction of response by CP 96,345, an NK selective non-peptide antagonist, and in part perhaps mediated by NK receptors. A small neurokinin receptor antagonist- and capsaicin-insensitive NANC contraction is probably not mediated by CGRP receptors. The α-adrenoceptor agonist oxymetazoline inhibited the evoked NANC response (22 nmol/1, IC; about 40%, maximum inhibition) without affecting the cholinergic response (up to 1 μmol/1) or the postjunctional iris sensitivity to exogenous substance P. The inhibition was antagonized by rauwolscine (apparent -log K 8.04) and by the relatively α-adrenoceptor selective antagonist ARC-239 (-log K 8.51). The α- and imidazoline receptor agonist aganodine inhibited the evoked NANC response (0.25 μmol/l, IC; about 30%, maximum inhibition) without affecting the postjunctional substance P responses. Rauwolscine 0.3 μmol/l failed to antagonize this effect. It is concluded that the release of sensory neurotransmitter(s) from trigeminal fibres in the rabbit eye may be inhibited by α-adrenoceptors and by a non-α-receptor, perhaps an imidazoline receptor. [ABSTRACT FROM AUTHOR] |
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