Characterization of capacitative calcium entry in submandibular gland acinar cells

Abstract

We studied an increase in the internal Ca concentration evoked the depletion of internal Ca stores (Ca-entry) with a SERCA inhibitor thapsigargin and/or a salivary gland secretagogue ACh in CD38 knockout (CD38 KO) mouse submandibular acinar cells. CD38 can generate cyclic ADP-ribose in the acinar cells. Thapsigargin evoked the Ca-entry divided into two phases, a rapid and a slow phase, equally in wild and CD38 KO cells. The elimination of CD38 greatly enhanced ACh induced Ca-entry. The presence of external Ni or excess of external K (90 mM) reduced the thapsigargin- and ACh-evoked Ca-entry. A phospholipase A₂ inhibitor 4-BPB (4-bromophenacyl bromide) enhanced the ACh-induced Ca-entry. The results suggest that the submandibular Ca-entry depends on the membrane potential, arachidonate formation , and the elimination of cyclic ADP-ribose. [Jpn J Physiol 54 Suppl:S70 (2004)]