cGMP abolishes agonist-induced [Ca2+]i oscillations in human bladder epithelial cells

被引:5
作者
Kwan, HY
Huang, Y
Kong, SK
Yao, X [1 ]
机构
[1] Chinese Univ Hong Kong, Fac Med, Dept Physiol, Hong Kong, Hong Kong, Peoples R China
[2] Chinese Univ Hong Kong, Fac Med, Dept Biochem, Hong Kong, Hong Kong, Peoples R China
关键词
protein kinase G; inositol 1,4,5-triphosphate; calcium release; nitric oxide; intracellular calcium concentration; guanosine; 3; 5 '-cyclic monophosphate;
D O I
10.1152/ajprenal.0031.2001
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Cytosolic calcium oscillations may permit cells to respond to information provided by increases in intracellular Ca2+ concentration ([Ca2+](i)) while avoiding prolonged exposure to constantly elevated [Ca2+](i). In this study, we demonstrated that agonists could induce Ca2+ oscillations in human bladder epithelial cells. Application of 10 muM acetylcholine or 200 nM bradykinin triggered an initial Ca2+ transient that was followed by periodic [Ca2+](i) oscillations. The oscillations did not depend on extracellular Ca2+. 8-Bromoguanosine 3', 5'-cyclic monophosphate abolished acetylcholine- or bradykinin-induced oscillations. Elevation of cellular cGMP by dipyridamole, an inhibitor of cGMP-specific phosphodiesterase, also terminated the [Ca2+](i) oscillations. The inhibitory effect of cGMP could be reversed by KT-5823, a highly specific inhibitor of protein kinase G (PKG), suggesting that the action of cGMP was mediated by PKG. Comparison of the effect of cGMP with that of xestospongin C, an inhibitor of the inositol 1,4,5-trisphosphate (IP3) receptor, revealed similarities between the action of cGMP and xestospongin C. Therefore, it is likely that cGMP and PKG may target a signal transduction step(s) linked to IP3 receptor-mediated Ca2+ release.
引用
收藏
页码:F1067 / F1074
页数:8
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