Effects of phosphorylation-related drugs on slow Ca2+ tail current in guinea-pig detrusor cells

Lorraine M. Smith, Shun Ichi Kajioka, Alison F. Brading, Shinsuke Nakayama

研究成果: ジャーナルへの寄稿記事

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In isolated guinea-pig detrusor cells, large conditioning depolarizations evoke slowly deactivating Ca2+ tail currents, considered to represent the second open state. The possible involvement of channel phosphorylation in this open state was examined. Application of isoprenaline caused a marginal increase in Ca2+ channel current evoked by simple depolarization, while forskolin did not. During application of either drug, slow-tail currents were never observed after simple depolarizations. The conditions necessary to induce slow-tail currents were not changed, even when cyclic AMP, ATP-γ-S (adenosine 5'-O-(3-thiotriphosphate)), GDP-β-S (guanosine 5'-O-(2-thiodiphosphate)) (in the pipette) or H-7 (1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride) (to the bathing solution) was applied. The frequent depolarization protocol, known to facilitate Ca2+ current via Ca2+ and cyclic AMP-dependent phosphorylation mechanism(s) in cardiac myocytes, did not induce slow-tail currents. These results suggest that the transition of Ca2+ channels to the second open state during large depolarization is not a result of (voltage-operated) channel phosphorylation itself. Possible underlying mechanisms are discussed. Copyright (C) 1999 Elsevier Science B.V.

元の言語英語
ページ(範囲)187-193
ページ数7
ジャーナルEuropean Journal of Pharmacology
370
発行部数2
DOI
出版物ステータス出版済み - 4 9 1999
外部発表Yes

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All Science Journal Classification (ASJC) codes

  • Pharmacology

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