Calcium is a crucial regulator of many physiological processes such as cell growth, division, differentiation, cell death and apoptosis. In this study, we examined the effect of cGMP on agonist-induced [Ca2+]i transient in isolated rat aortic endothelial cells. 100 μM ATP was applied to the cells bathed in a Ca2+-free physiological solution to induce a [Ca2+]i transient that was caused by Ca2+ release from intracellular stores. cGMP, which was applied after [Ca2+]i reached its peak level, accelerated the falling phase of [Ca2+]i transient. Pre-treatment of the cells with CPA abolished the accelerating effect of cGMP on the falling phase of [Ca2+]i transient. The effect of cGMP was reversed by KT5823, a highly specific inhibitor of protein kinase G. Taken together, these data suggest that cGMP may reduce [Ca2+]i level by promoting Ca2+ uptake through sarcoplasmic/endoplasmic reticulum ATPase and that the effect of cGMP may be mediated by protein kinase G.
Scopus Subject Areas
- Biochemistry, Genetics and Molecular Biology(all)
- Pharmacology, Toxicology and Pharmaceutics(all)
- Endothelial cells