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Mechanism of action of nicotine in isolated iris sphincter preparations of rabbit
Author(s) -
Hisayama Tetsuhiro,
Shinkai Michiko,
Takayanagi Issei,
Morimoto ShinIchi,
Ishida Katsuko
Publication year - 1988
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1988.tb11666.x
Subject(s) - hexamethonium , nicotine , atropine , tetrodotoxin , acetylcholine , contraction (grammar) , chemistry , endocrinology , medicine , pharmacology , capsaicin , substance p , neuropeptide , receptor
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 ‐Arg 1 , d ‐Pro 2 , d ‐Trp 7,9 , Leu 11 ]‐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.