title: Effect of osmolality on cytosolic free calcium and aldosterone secretion.
abstract: Alterations in extracellular osmolality have powerful inverse effects on basal and potassium- and angiotensin-stimulated aldosterone secretion. With the use of bovine glomerulosa cells grown in primary culture, the effects of alterations in osmolality on cytosolic calcium concentration ([Ca2+]c), efflux and uptake of 45Ca2+, and aldosterone secretion were determined. Alterations in osmolality, independent of sodium concentration, have inverse effects on aldosterone secretion, which are correlated with simultaneous changes in [Ca2+]c measured using fura-2. Reductions in osmolality cause dose-dependent biphasic increases in [Ca2+]c different from the monophasic increases in [Ca2+]c produced by increases in potassium concentration. Like potassium- and angiotensin-stimulated increases in [Ca2+]c, hypotonically induced increases in [Ca2+]c are associated with an increase in 45Ca2+ efflux. Reductions in osmolality also increased the uptake of 45Ca2+, an effect apparent at 2 min and persistent for at least 30 min. In the absence of extracellular calcium, reductions in osmolality, as increases in potassium concentration but not angiotensin, fail to increase [Ca2+]c, efflux of 45Ca2+, or aldosterone secretion. In conclusion, osmolality-induced alterations in aldosterone secretion are associated with parallel changes in [Ca2+]c, effects caused by alteration in the influx of extracellular calcium. On the basis of these and previous studies, we hypothesize that osmolality affects calcium influx by activating voltage-dependent or stretch-activated calcium channels.
authors.affiliation: Department of Physiology and Biophysics, University of Tennessee, Memphis 38163.
authors.forename: W
authors.initials: W
authors.lastname: Wang
authors.forename: N
authors.initials: N
authors.lastname: Hayama
authors.forename: T V
authors.initials: TV
authors.lastname: Robinson
authors.forename: R E
authors.initials: RE
authors.lastname: Kramer
authors.forename: E G
authors.initials: EG
authors.lastname: Schneider
mesh_terms: D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D003600:Cytosol / Q000378:metabolism*; D005110:Extracellular Space / Q000378:metabolism; D009994:Osmolar Concentration; D011188:Potassium / Q000494:pharmacology; D015384:Zona Glomerulosa / Q000166:cytology / Q000378:metabolism
chemical_list: D000804:Angiotensin II; D000450:Aldosterone; D011188:Potassium; D002118:Calcium