Ca2+ entry through the store-mediated pathway directly activates only the K+ current but the subsequent Ca2+ release from the store activates both K+ and Cl- currents in submandibular gland acinar cells of the rat

• Published in: Cellular signalling Vol. 7; no. 8; pp. 783 - 791
• Main Authors: Wakui, M, Wada, J, Kamimura, N, Mio, Y, Sasaki, T, Fukushi, Y, Nishiyama, A
• Format: Journal Article
• Language: English
• Published: England 01.11.1995
• Subjects: Acetylcholine - pharmacology; Animals; Biological Transport - drug effects; Calcium - metabolism; Calcium Channel Blockers - pharmacology; Calcium Channels - drug effects; Calcium Channels - metabolism; Cell Compartmentation; Chlorides - metabolism; Imidazoles - pharmacology; Inositol Phosphates - metabolism; Nifedipine - pharmacology; Patch-Clamp Techniques; Potassium - metabolism; Rats; Signal Transduction - drug effects; Submandibular Gland - drug effects; Submandibular Gland - metabolism
• ISSN: 0898-6568; 1873-3913
• DOI: 10.1016/0898-6568(95)02006-3

The store-mediated Ca2+ entry was detected in single and cluster of rat submandibular acinar cells by measuring the Ca2+ activated ionic membrane currents. In the cells where intracellular Ca2+ was partly depleted by stimulation with submaximal concentration of acetylcholine (ACh) under a Ca2(+)-free extracellular condition, an employment of external Ca2+ in the absence of ACh caused a sustained increase of the K+ current without affecting the Cl- current. A renewed ACh challenge without external Ca2+ caused repetitive spikes of both K+ and Cl- currents due to the Ca2+ release. SK & F 96365 inhibited the generation of the sustained K+ current and refilling of the Ca2+ store following the Ca2+ readmission. It is suggested that the Ca2+ enters the cell through the store-mediated pathway new the K+ channels and is taken up by the store. Thus, only Ca2+ released from the store can activate both the K+ and Cl- currents.