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. 1996 Nov 15;497(Pt 1):19–29. doi: 10.1113/jphysiol.1996.sp021746

Anion secretion induced by capacitative Ca2+ entry through apical and basolateral membranes of cultured equine sweat gland epithelium.

W H Ko 1, H C Chan 1, P Y Wong 1
PMCID: PMC1160909  PMID: 8951708

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.

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Selected References

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