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PROBING EXCITATION‐CONTRACTION COUPLING IN TRACHEALIS SMOOTH MUSCLE WITH THE MYCOTOXIN CYCLOPIAZONIC ACID
Author(s) -
Amoako Daniel,
Qian Yun,
Kwan ChiuYin,
Bourreau JeanPierre
Publication year - 1996
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1996.tb01768.x
Subject(s) - trachealis muscle , chemistry , contraction (grammar) , cyclopiazonic acid , biophysics , tonic (physiology) , acetylcholine , muscle contraction , stimulation , channel blocker , membrane potential , medicine , charybdotoxin , intracellular , biochemistry , calcium , biology , organic chemistry
SUMMARY 1. Muscarinic stimulation‐induced tonic contraction of airway smooth muscle is independent of membrane potential. This contraction is not sensitive to inhibition by voltage‐operated Ca 2+ channel blockers or by K + channel openers. 2. Cyclopiazonic acid (CPA) inhibits Ca 2+ loading of internal stores but does not affect maximal tonic contraction induced by acetylcholine (ACh) in steady state conditions. 3. After depletion of internal Ca 2+ stores with CPA, AChinduced tonic contraction becomes dependent upon values of membrane potential. The contraction is then sensitive to voltage‐operated Ca 2+ channel blockers and to K + channel openers. 4. Treatment of trachealis muscle with CPA potentiates the M 2 ‐mediated component of ACh stimulation, but this potentiation is not entirely responsible for the switch in excitation‐contraction (E‐C) coupling. 5. It is proposed that depletion of internal Ca 2+ stores with CPA and promotion of M 2 ‐stimulation can lead to a switch in E‐C coupling in trachealis smooth muscle from pharmaco‐ to electromechanical mode, perhaps by targeting a plasma membrane K + channel.