Ca²⁺ entry pathways in rat submandibular acinar cells

Abstract

Ca²⁺ entry pathways in rat submandibular acinar cellsYoshida, H. and Nakahari, T.Department of Physiology, Osaka Medical College, 2-7 Daigaku-cho, Takatsuki 569-8686, JapanIn rat submandibular acinar cells, ACh evoked a biphasic increase in [Ca²⁺]_i, that is, an initial transient phase followed by a sustained phase. The initial transient phase is induced by a Ca²⁺ release from the intracellular stores and the sustained phase is maintained by a Ca²⁺ influx from the extracellular fluid, which is triggered by empty stores and is the so-called "store-operated Ca²⁺ entry". Store-operated Ca²⁺ entry was stimulated using 4 microM thapsigargin, sarco(end)plasmic reticulum Ca²⁺ ATPase inhibitor, in Ca²⁺-free solution (no added Ca²⁺ + 1mM EGTA) followed by superfusion with control (Ca²⁺-containing) solution. This protocol resulted in a [Ca²⁺]_i increase, which was inhibited in the presence of 100 microM Gd³⁺, 100microM La³⁺ but was unaffected by addition of 1 microM Gd³⁺ or 10 microM H-89, PKA inhibitor. A restoration from a high K+ solution(Ca²⁺-containing) to control solution also evoked an [Ca²⁺]_i increase during thapsigargin stimulation, and an [Ca²⁺]_i increase following reintroduction of Ca²⁺ during thapsigargin stimulation was completely inhibited by addition of 1 microM Gd³⁺ but was partially affected by addition of 10 microM H-89 . Thus, one effect of the reintroduction of Ca²⁺ is likely to be a hyperpolarization voltage. In conclusion, rat submandibular acinar cells have at least two Ca²⁺ entry pathways; one is activated by the store-depletion, and the other is by cAMP and hyperpolarization. [Jpn J Physiol 54 Suppl:S89 (2004)]