AJP - Cell Physiology, Vol 266, Issue 4 C1006-C1012, Copyright © 1994 by American Physiological Society

ARTICLES

Calcium signaling induced by bradykinin is synergistically enhanced by high K+ in NG108-15 cells

S. H. Chueh and L. S. Kao
Department of Biochemistry, National Defense Medical Center, Academia Sinica, Taipei, Taiwan, Republic of China.

We report a novel phenomenon in which the cytosolic Ca2+ concentration ([Ca2+]i) rise induced in neuroblastoma x glioma hybrid NG108-15 cells by bradykinin is synergistically enhanced by elevated extracellular K+ concentrations. Presence of extracellular Ca2+ during high-K+ treatment, but not after high-K+ treatment, was required for the synergism. In addition, when thapsigargin was added concurrently with high K+, bradykinin still induced a significantly higher [Ca2+]i rise than in cells treated with thapsigargin only. Both bradykinin-induced inositol 1,4,5-trisphosphate (IP3) generation and the size of the internal Ca2+ pool were increased by high-K+ treatment. Our data suggest that changes in membrane potential itself induced by high K+ probably do not cause the synergistic effect. The synergistic effect is apparently due to the stimulatory effects of high K+ on [Ca2+]i, which in turn modulates IP3 generation and increases the size of intracellular Ca2+ pools. If bradykinin is added following high K+, the synergism can be accounted for by increases both in IP3 production and in the size of the internal Ca2+ pools. If bradykinin is added simultaneously with high K+, enhanced Ca2+ release triggered by enhanced IP3 production is the major cause of the synergistic effects.

This article has been cited by other articles:

				T.-Y. Chin, H.-M. Hwang, and S.-H. Chueh Distinct Effects of Different Calcium-Mobilizing Agents on Cell Death in NG108-15 Neuroblastoma X Glioma Cells Mol. Pharmacol., March 1, 2002; 61(3): 486 - 494. [Abstract] [Full Text] [PDF]