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Spasmogen action in guinea‐pig isolated trachealis: involvement of membrane K + ‐channels and the consequences of K + ‐channel blockade
Author(s) -
Boyle J.P.,
Davies J.M.,
Foster R.W.,
Good D.M.,
Kennedy I.,
Small R.C.
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.tb11437.x
Subject(s) - trachealis muscle , chemistry , tetraethylammonium , depolarization , procaine , histamine , membrane potential , tetraethylammonium chloride , biophysics , acetylcholine , endocrinology , medicine , anesthesia , potassium , biochemistry , charybdotoxin , biology , organic chemistry
1 Acetylcholine (ACh), histamine, prostaglandin E 2 and potassium chloride (KCl) each evoked concentration‐dependent spasm of guinea‐pig isolated trachealis treated with indomethacin (2.8 μ m ). 2 Neither tetraethylammonium (TEA; 0.1–10 m m ) nor procaine (0.1–10 m m ) potentiated these spasmogens. Indeed, procaine (10 m m ) depressed the log concentration‐effect curves of all the spasmogens while TEA (1–10 m m ) caused some depression of the log concentration‐effect curve of prostaglandin E 2 . 3 Intracellular electrophysiological recording was performed in trachealis bathed by normal Krebs solution or by Krebs solution containing 2.8 μ m indomethacin. In either medium the majority of trachealis cells exhibited spontaneous electrical slow waves while some cells were electrically quiescent. In either medium the spasmogenic effects of ACh (1 m m ) and histamine (0.2 m m ) were accompanied by depolarization and abolition of slow wave discharge. In many cases the record of membrane potential subsequently exhibited noise which incorporated fast, hyperpolarizing transients. 4 In the absence and presence of indomethacin, TEA (10 m m ) and procaine (5 m m ) markedly reduced the membrane noise and hyperpolarizing transients evoked by ACh or histamine without augmenting the evoked tension. 5 It is concluded that slow wave discharge does not depend on prostaglandin synthesis. The membrane noise and hyperpolarizing transients evoked by ACh and histamine represent the opening of membrane K + ‐channels. While such K + ‐channel opening may offset spasmogen‐induced depolarization it does not moderate the evoked tension.