Modulation of Ca2+ -sensitivity for contraction in canine tracheal smooth muscle

To investigate the regulatory mechanisms of Ca^2+ -sensitivity for contraction in airway smooth muscle, we permeabilized canine tracheal smooth muscle(CTSM) with staphylococcus aureus α-toxin (5000IU/mL, 30℃, 30-45min), and measured isometric force. pCa6.7-induced submaximal contractions (7.3±2% of...

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Published inJapanese Journal of Pharmacology Vol. 71; no. suppl.1; p. 209
Main Authors Iizuka, Kunihiko, Dobashi, Kunio, Nakazawa, Tsugio, Mori, Masatomo
Format Journal Article
LanguageEnglish
Published The Japanese Pharmacological Society 1996
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Abstract To investigate the regulatory mechanisms of Ca^2+ -sensitivity for contraction in airway smooth muscle, we permeabilized canine tracheal smooth muscle(CTSM) with staphylococcus aureus α-toxin (5000IU/mL, 30℃, 30-45min), and measured isometric force. pCa6.7-induced submaximal contractions (7.3±2% of max., S.E.M., n=3~4) were augmented by either 100μM carbachol (22.2±2%) or 10μM AlF_4 ^- (61.7± 3%) at constant free Ca^2+ (10mM EGTA at 24℃). They were reversed by 10μM atropine (103±7% of the carbachol-induced augmentation) or 3mM GDPβS (87.6±7% of the AlF_4 ^- -induced augmentation), respectively. 100μM NKH477, a water soluble forskolin, relaxed the pCa6.7 plus 30μM GTPγS-induced contraction by 64.8±4% (n=3), and 100~300μM 8-BrcAMP, a cAMP analogue, relaxed the contraction 2+ almost completely. These results indicate that Ca^2+ -sensitivity in CTSM is increased by receptor coupled, trimeric G-protein(s)-involved mechanisms and decreased by the signaling through adenylate cyclase.
AbstractList To investigate the regulatory mechanisms of Ca^2+ -sensitivity for contraction in airway smooth muscle, we permeabilized canine tracheal smooth muscle(CTSM) with staphylococcus aureus α-toxin (5000IU/mL, 30℃, 30-45min), and measured isometric force. pCa6.7-induced submaximal contractions (7.3±2% of max., S.E.M., n=3~4) were augmented by either 100μM carbachol (22.2±2%) or 10μM AlF_4 ^- (61.7± 3%) at constant free Ca^2+ (10mM EGTA at 24℃). They were reversed by 10μM atropine (103±7% of the carbachol-induced augmentation) or 3mM GDPβS (87.6±7% of the AlF_4 ^- -induced augmentation), respectively. 100μM NKH477, a water soluble forskolin, relaxed the pCa6.7 plus 30μM GTPγS-induced contraction by 64.8±4% (n=3), and 100~300μM 8-BrcAMP, a cAMP analogue, relaxed the contraction 2+ almost completely. These results indicate that Ca^2+ -sensitivity in CTSM is increased by receptor coupled, trimeric G-protein(s)-involved mechanisms and decreased by the signaling through adenylate cyclase.
Author Kunio Dobashi
Kunihiko Iizuka
Masatomo Mori
Tsugio Nakazawa
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