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 |
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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. |
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ISSN: | 0363-6143 0002-9513 1522-1563 |
DOI: | 10.1152/ajpcell.1996.271.6.C1935 |