title: Anion secretion induced by capacitative Ca2+ entry through apical and basolateral membranes of cultured equine sweat gland epithelium.
abstract: 1. Anion secretion induced by capacitative Ca2+ entry through apical and basolateral membranes of cultured equine sweat gland epithelium was studied using the short-circuit current (Isc) technique. 2. Thapsigargin induced an increase in Isc that could be inhibited when external Ca2+ was chelated by EGTA. 3. The inhibition of the thapsigargin-induced Isc could be reversed by re-addition of Ca2+ to apical or basolateral solutions. The magnitude of the reactivated Isc depended predominantly on basolateral Ca2+ concentration. 4. The magnitude of the reactivated Isc upon basolateral Ca2+ addition increased with the thapsigargin concentration, indicating its dependence on the emptied state of the Ca2+ store induced by thapsigargin. 5. The thapsigargin-induced Isc, as well as the Ca(2+)-dependent reactivation of Isc in EGTA-treated epithelia, was inhibitable by apical, but not basolateral, addition of flufenamate, and by basolateral addition of La3+. Other Ca2+ channel blockers, verapamil and nifedipine, had no effect when applied to either membrane. 6. The results suggest that thapsigargin-induced anion secretion by the equine sweat gland epithelial cells is crucially dependent upon the Ca2+ influx occurring primarily through the basolateral membrane, and that apical and basolateral membranes may possess different pathways for Ca2+ entry.
authors.affiliation: Department of Physiology, Faculty of Medicine, Chinese University of Hong Kong, Shatin, NT, Hong Kong. whko@cuhk.edu.hk
authors.forename: W H
authors.initials: WH
authors.lastname: Ko
authors.forename: H C
authors.initials: HC
authors.lastname: Chan
authors.forename: P Y
authors.initials: PY
authors.lastname: Wong
mesh_terms: D000818:Animals; D000838:Anions / Q000378:metabolism*; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002462:Cell Membrane / Q000378:metabolism; D002478:Cells, Cultured; D002614:Chelating Agents / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D004594:Electrophysiology; D005439:Flufenamic Acid / Q000494:pharmacology; D006736:Horses; D007476:Ionophores / Q000494:pharmacology; D007811:Lanthanum / Q000494:pharmacology; D013545:Sweat Glands / Q000378:metabolism*; D019284:Thapsigargin / Q000494:pharmacology
chemical_list: D000838:Anions; D002614:Chelating Agents; D007476:Ionophores; D000001:Calcimycin; D004533:Egtazic Acid; D005439:Flufenamic Acid; D019284:Thapsigargin; D007811:Lanthanum; D002118:Calcium