Basic properties of a novel ryanodine-sensitive, caffeine-insensitive calcium-induced calcium release mechanism in permeabilised human vascular smooth muscle cells.

The efflux of 45Ca2+ from preloaded intracellular stores of saponin-permeabilised human uterine artery smooth muscle cultured cells was used to study the mechanisms underlying Ca2+ release from the sarcoplasmic reticulum (SR). The present paper demonstrates directly a functional Ca2+ release mechanism that is dependent on an increase in free Ca2+ (100 nM-30 microM) and is completely inhibited by 20 microM Ruthenium red. The amount of Ca2+ released at 30 microM free Ca2+ was reduced by approximately 50% compared to the release at 10 microM. This Ca(2+)-induced Ca2+ release (CICR) mechanism was not sensitive to caffeine. Exposure of cells to low free Ca(2+)-containing solutions (10 nM) indicated that a component of the CICR mechanism may be functional at basal free Ca2+ levels of 100 nM. Application of ryanodine (0.1-100 microM) induced 45Ca2+ efflux from the sarcoplasmic reticulum and this release was also inhibited by 20 microM Ruthenium red.