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Am J Physiol Cell Physiol 275: C571-C580, 1998;
0363-6143/98 $5.00
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Vol. 275, Issue 2, C571-C580, August 1998

Regulation of KCa current by store-operated Ca2+ influx depends on internal Ca2+ release in HSG cells

Xibao Liu1, Eduardo Rojas2, and Indu S. Ambudkar1

1 Secretory Physiology Section, Gene Therapy and Therapeutics Branch, National Institute of Dental Research, and 2 Laboratory of Cell Biology and Biochemistry, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892

This study examines the Ca2+ influx-dependent regulation of the Ca2+-activated K+ channel (KCa) in human submandibular gland (HSG) cells. Carbachol (CCh) induced sustained increases in the KCa current and cytosolic Ca2+ concentration ([Ca2+]i), which were prevented by loading cells with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). Removal of extracellular Ca2+ and addition of La3+ or Gd3+, but not Zn2+, inhibited the increases in KCa current and [Ca2+]i. Ca2+ influx during refill (i.e., addition of Ca2+ to cells treated with CCh and then atropine in Ca2+-free medium) failed to evoke increases in the KCa current but achieved internal Ca2+ store refill. When refill was prevented by thapsigargin, Ca2+ readdition induced rapid activation of KCa. These data provide further evidence that intracellular Ca2+ accumulation provides tight buffering of [Ca2+]i at the site of Ca2+ influx (H. Mogami, K. Nakano, A. V. Tepikin, and O. H. Petersen. Cell 88: 49-55, 1997). We suggest that the Ca2+ influx-dependent regulation of the sustained KCa current in CCh-stimulated HSG cells is mediated by the uptake of Ca2+ into the internal Ca2+ store and release via the inositol 1,4,5-trisphosphate-sensitive channel.

calcium-activated potassium channel; store-operated calcium influx; salivary gland cells; muscarinic receptor


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