Evidence for an intracellular calcium store releasable by surface stimuli ifibroblasts (L cells).

Abstract

A spontaneously occurring or electrically elicited hyperpolarizing activation (HA) in L cells is due to a specific increase in the membrane K+ permeability. Intracellular injection of Ca2+ elicits an identical hyperpolarizing response which suggests that the increased K+ permeability associated with the HA is mediated by an increase in cytoplasmic Ca2+. In Ca free, EGTA[ethylene glycol tetraacetic acid]-containing saline the proportion of cells in which HA can be evoked decreases, but the amplitude of HA produced is comparable to that of HA in normal Ca-containing saline. Co2+ blocks HA but only after a period of 2 h or longer; D-600 [.alpha.-isopropyl-.alpha.[(N-methyl-N-homoveratryl)-.gamma.-aminopropyl]-3,4,5-trimethoxyphenyl-acetonitrile] does not affect the HA. The primary source of the Ca mediating the HA response may be intracellular. In L cells, the endoplasmic reticulum forms morphologically specialized appositions with the surface membrane resembling structures at the triads of muscle that may mediate coupling between surface membrane electrical activity and contraction via Ca release from the sarcoplasmic reticulum. The similar structures in L cells may mediate coupling between surface membrane electrical, mechanical or chemical stimuli and the HA response via release of Ca from the endoplasmic reticulum. Surface-coupled release of Ca from intracellular stores might also regulate other intracellular functions in nonmusucle cells.