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. 1988 Oct;95(2):459–464. doi: 10.1111/j.1476-5381.1988.tb11666.x

Mechanism of action of nicotine in isolated iris sphincter preparations of rabbit.

T Hisayama 1, M Shinkai 1, I Takayanagi 1, S Morimoto 1, K Ishida 1
PMCID: PMC1854194  PMID: 3228672

Abstract

1. Nicotine produced a transient contraction of rabbit isolated iris sphincter muscle, a parasympathetic ganglion-free tissue. The response to nicotine was antagonized by hexamethonium, but was insensitive to tetrodotoxin (TTX). While single treatments with atropine, capsaicin or [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-substance P (rpwwL-SP) partially blocked the response, combined treatment abolished it. 2. Chronic treatment of animals with nicotine added to the drinking water (about 12 mg kg-1 per day) had no effect on the responsiveness to nicotine or the pharmacological properties of nicotine-induced contraction. 3. These results suggest that acetylcholine and tachykinin(s) released via sodium channel-independent mechanisms from nerve terminals of parasympathetic and primary sensory nerves, respectively, are involved in the nicotine-induced contractile response.

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Selected References

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