Yoshimoto R, Hori M, Takahashi K, Taniguchi S I, Katsuki M, Ozaki H, Karaki H
Department of Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Japan.
Jpn J Pharmacol. 2000 Dec;84(4):474-5. doi: 10.1254/jjp.84.474.
Role of h1 calponin on Ca2+-sensitivity of smooth muscle contraction was investigated using h1 calponin gene-deficient mice (CP -/-) and wild type mice (CP +/+). PGF2. induced a comparable force in intact aorta of CP +/+ and CP -/-. DPB showed similar effects to PGF2alpha. In membrane-permeabilized ileal smooth muscle, PDBu enhanced Ca2+-sensitivity of contraction comparably in CP +/+ and CP -/-. GTPgamma-S showed similar effects. Our results suggest that h1 calponin does not regulate Ca2+-sensitivity in the contractile mechanism of smooth muscle.
利用h1钙调蛋白基因缺陷小鼠(CP -/-)和野生型小鼠(CP +/+)研究了h1钙调蛋白对平滑肌收缩的Ca2+敏感性的作用。PGF2α在CP +/+和CP -/-的完整主动脉中诱导出相当的张力。二丁酰环磷腺苷(DPB)显示出与PGF2α相似的作用。在膜通透的回肠平滑肌中,佛波醇酯(PDBu)在CP +/+和CP -/-中对收缩的Ca2+敏感性增强作用相当。鸟苷-5'-O-(3-硫代三磷酸)(GTPγ-S)显示出相似的作用。我们的结果表明,h1钙调蛋白在平滑肌收缩机制中不调节Ca2+敏感性。