AJP - Cell Physiology, Vol 268, Issue 6 C1485-C1491, Copyright © 1995 by American Physiological Society

ARTICLES

Inositol phosphate structural requisites for Ca2+ influx

S. DeLisle, G. W. Mayr and M. J. Welsh
Veterans Affairs Medical Center, Iowa City, Iowa, USA.

To understand how inositol phosphates (InsP) cause Ca2+ influx, we injected 37 highly purified compounds containing a total of 49 InsP positional isomers into Xenopus oocytes. The eight InsP that stimulated Ca2+ influx were those that had the highest potency at releasing intracellular Ca2+, indicating that their common target was the inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] receptor. To cause Ca2+ influx, these InsP had to be injected in a much higher concentration than the minimal concentration required to release intracellular Ca2+. Such high InsP concentrations could inhibit ongoing oscillatory intracellular Ca2+ release. In addition, we found that InsPs could not elicit further intracellular Ca2+ release during the course of Ca2+ influx. Our data are consistent with the "capacitative Ca2+ entry" hypothesis, which states that InsP stimulate Ca2+ influx by depleting the InsP-sensitive intracellular Ca2+ store. In this context, we would suggest that to deplete the InsP-sensitive intracellular Ca2+ store, InsP may have to be present in a sufficiently high concentration to override the oscillatory Ca(2+)-refilling mechanisms of the stores.

This article has been cited by other articles:

				H. C. Hartzell, K. Machaca, and Y. Hirayama Effects of Adenophostin-A and Inositol-1,4,5-trisphosphate on Cl- Currents in Xenopus laevis Oocytes Mol. Pharmacol., April 1, 1997; 51(4): 683 - 692. [Abstract] [Full Text]