Agonist-induced entry of Ca(2+) in smooth muscle cells.
The changes in intracellar Ca(2+)-concentration, which occur during stimulation of vascular smooth muscle cells with excitatory agonists, are discussed. The effects of these agonists on the membrane potential of these cells are indirect, and mainly due to an activation of K(+)- and Cl(?)-channels by the release of calcium from internal stores. Voltage-dependent Ca(2+)-channels are only activated if the cells depolarize beyond the threshold for activation of these channels. However, the influx of calcium through these channels is strongly inhibited by the agonists, probably via activation of protein kinase C. The mechanism of agonist-mediated Ca(2+)-entry is shown to be modulated by the degree of Ca(2+)-depletion of the agonist-sensitive Ca(2+)-stores. Arguments are presented in favour of a direct pathway for Ca(2+)-entry from the extracellular medium into this agonist-sensitive store.
Casteels
R
R
Physiological Laboratory, University of Leuven, B-3000 Leuven, Belgium.
Droogmans
G
G
Missiaen
L
L