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Rapid and non‐genomic reduction of intracellular [Ca 2+ ] induced by aldosterone in human bronchial epithelium
Author(s) -
Urbach Valérie,
Harvey Brian J.
Publication year - 2001
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2001.0267k.x
Subject(s) - thapsigargin , aldosterone , medicine , endocrinology , cyclase , adenylate kinase , chemistry , ouabain , fura 2 , biology , intracellular , microbiology and biotechnology , biochemistry , stimulation , sodium , enzyme , organic chemistry , cytosol
1 Using a Ca 2+ imaging system and fura‐2 AM (5 μ m ) we showed that exposure of polarised monolayers of human bronchial epithelial cells (16HBE14o‐ cell line) to aldosterone produced a fast intracellular [Ca 2+ ] ([Ca 2+ ] i ) decrease, in 70 % of cells. Exposure to aldosterone (1 n m ) reduced the [Ca 2+ ] i by 39 ± 9 n m ( n = 282, P < 0.0001) within 10 min, from a basal [Ca 2+ ] i of 131 ± 19 n m ( n = 282). 2 The effect of aldosterone on [Ca 2+ ] i was not affected by inhibitors of the classical genomic pathway, cycloheximide (1 μ m ) or spironolactone (10 μ m ). The aldosterone‐induced [Ca 2+ ] i decrease was inhibited by thapsigargin (1 μ m ), pertussis toxin (24 h at 200 ng ml −1 ), the adenylate cyclase inhibitors 2′,3′‐dideoxyadenosine (200 μ m ) and MDL‐12,330A hydrochloride (500 μ m ), and the protein kinase A inhibitor R P ‐adenosine 3′,5′‐cyclic monophosphorothioate (200 μ m ). In addition, treatment of 16HBE14o‐ monolayers with aldosterone (1 n m ) inhibited by ≈30 % the large and transient [Ca 2+ ] i increase induced by apical exposure to uridine triphosphate (UTP, 0.1 m m ), a known secretagogue in airway epithelia. 3 Our results demonstrate for the first time that in human bronchial epithelial cells, aldosterone decreases [Ca 2+ ] i levels via a non‐genomic mechanism. The hormone‐induced changes to [Ca 2+ ] i involve stimulation of thapsigargin‐sensitive Ca 2+ ‐ATPase, via G‐protein‐, adenylate cyclase‐ and protein kinase A‐coupled signalling pathways.