二丁酰环磷腺苷和福斯高林抑制血管平滑肌中的磷脂酰肌醇水解、钙离子内流及收缩。

Dibutyryl cyclic AMP and forskolin inhibit phosphatidylinositol hydrolysis, Ca2+ influx and contraction in vascular smooth muscle.

作者信息

Ahn H Y, Kang S E, Chang K C, Karaki H

机构信息

Department of Pharmacology, College of Medicine, Chungbuk National University, Cheongju, Korea.

出版信息

Jpn J Pharmacol. 1992 Jun;59(2):263-5. doi: 10.1254/jjp.59.263.

DOI:10.1254/jjp.59.263

PMID:1331585

Abstract

Dibutyryl cyclic AMP and forskolin inhibited the contraction induced by norepinephrine (NE) more strongly than the high K(+)-induced contraction in isolated rat aorta. These inhibitors inhibited the 45Ca2+ influx stimulated by NE but not that by high K+, and they inhibited NE-induced inositol monophosphate accumulation. These results suggest that cAMP inhibits NE-induced contraction, at least partly, by inhibiting the alpha-adrenoceptor-mediated signal transduction and high K(+)-induced contraction by decreasing Ca2+ sensitivity but not Ca2+ influx.

摘要

在离体大鼠主动脉中，二丁酰环磷腺苷（Dibutyryl cyclic AMP）和福斯高林（forskolin）对去甲肾上腺素（NE）诱导的收缩的抑制作用比对高钾（K⁺）诱导的收缩更强。这些抑制剂抑制了NE刺激的⁴⁵Ca²⁺内流，但不抑制高钾刺激的⁴⁵Ca²⁺内流，并且它们抑制了NE诱导的肌醇单磷酸积累。这些结果表明，环磷腺苷（cAMP）至少部分地通过抑制α-肾上腺素能受体介导的信号转导来抑制NE诱导的收缩，并且通过降低Ca²⁺敏感性而非Ca²⁺内流来抑制高钾（K⁺）诱导的收缩。