Rapid effects of steroid hormones on free intracellular calcium in T84 colonic epithelial cells

C. M. Doolan and B. J. Harvey Wellcome Trust Cellular Physiology Research Unit, Department of Physiology, University College, Cork, Ireland. Studies from our laboratory have demonstrated rapid (< 1 min) nongenomic activation of K+ recycling and Na+/H+ exchange by mineralocorticoids in human colon...

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Veröffentlicht in:American Journal of Physiology: Cell Physiology 1996-12, Vol.271 (6), p.C1935-C1941
Hauptverfasser: Doolan, C. M, Harvey, B. J
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Sprache:eng
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Zusammenfassung:C. M. Doolan and B. J. Harvey Wellcome Trust Cellular Physiology Research Unit, Department of Physiology, University College, Cork, Ireland. Studies from our laboratory have demonstrated rapid (< 1 min) nongenomic activation of K+ recycling and Na+/H+ exchange by mineralocorticoids in human colonic epithelium, and studies from other laboratories have demonstrated rapid effects of aldosterone on intracellular Ca2+ concentration ([Ca2+]i) in endothelial cells. Here a rapid nongenomic effect of aldosterone on [Ca2+]i is demonstrated in the human colonic epithelial cell line T84. Aldosterone induced a rapid increase in [Ca2+]i within approximately 2 min. The rise in [Ca2+]i after aldosterone appears to result from the activation of a Ca2+ influx pathway, inasmuch as 1) no increase in [Ca2+]i was observed with aldosterone when cells were bathed in Ca(2+)-free Krebs solution and 2) emptying of the intracellular Ca2+ stores by thapsigargin was not enhanced by addition of aldosterone to extracellular Ca(2+)-free solution. In contrast, the Ca2+ response to aldosterone, in the presence of 2 mM Ca2+ in the external bathing solution, was not decreased after intracellular Ca2+ stores were emptied by thapsigargin. Other mineralocorticoid hormones increased [Ca2+]i, whereas the glucocorticoid hydrocortisone failed to increase [Ca2+]i. These results demonstrate the existence of a mineralocorticoid-specific Ca(2+)-signaling pathway in human colonic T84 (crypt) epithelial cells.
ISSN:0363-6143
0002-9513
1522-1563
DOI:10.1152/ajpcell.1996.271.6.C1935