Author:

Keywords:

Adenosine Triphosphate, Animals, Aorta, Thoracic, Calcium, Cell Line, Inositol 1,4,5-Trisphosphate, Kinetics, Muscle, Smooth, Vascular, Rats, Research Support, Non-U.S. Gov't, Science & Technology, Life Sciences & Biomedicine, Physiology, Ca2+ stores, IP3 receptor, intracellular Ca2+ release, INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR, CALCIUM-RELEASE, CYTOSOLIC CA2+, TRISPHOSPHATE, ELEMENTARY, CEREBELLUM, CHANNELS, 0606 Physiology, 1106 Human Movement and Sports Sciences, 1116 Medical Physiology, 3101 Biochemistry and cell biology, 3109 Zoology, 3208 Medical physiology

Abstract:

There is still no agreement on the mechanism of the intracellular action of low concentrations of inositol 1,4,5-trisphosphate (IP3). Intracellular Ca2+ stores may transiently release some Ca2+ before they become insensitive to IP3. Alternatively, stores with a low IP3 threshold may lose all their Ca2+ and the others none. We now report that the IP3 threshold was not correlated with the extent of Ca2+ release in permeabilized A7r5 smooth-muscle cells. In contrast, the maximum rate of release, which was changed either by varying the level of IP3 receptor (IP3R) activation, or by changing the concentration of IP3R at a constant level of IP3R activation, was directly related to the extent of Ca2+ release. We conclude that IP3-induced Ca2+ release reflects partial emptying of the stores and not all-or-none Ca2+ release of separate quanta.