HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Spät, A. Articles by Hunyady, L. Search for Related Content PubMed PubMed Citation Articles by Spät, A. Articles by Hunyady, L.

Initial ⁴⁵Ca uptake was measured in isolated rat glomerulosa cells. A small reduction in membrane potential produced by increasing the K⁺ concentration from 2 to 3·6 mmol/l stimulated ⁴⁵Ca uptake by about 35%, while a bigger depolarization induced by 18·5 mmol K⁺/l increased the uptake by about 100%. Since Ca²⁺ influx was already activated at a calculated membrane potential below –70 mV, and was found to be sensitive to the dihydropyridine antagonist nifedipine (1 µmol/l), but insensitive to nickel ions (100 µmol/l), it does not meet the criteria established for T- or L-type voltage-dependent Ca²⁺ channels. Exposure of glomerulosa cells to angiotensin II (AII) for 10 min also enhanced the rate of ⁴⁵Ca influx. The effect of AII was not sensitive to 1 µmol nifedipine/l, but was strongly inhibited by 5-(N-4-chlorobenzyl)-N-(2',4'-dimethyl)benzamil (CBDMB, 30 µmol/l), an inhibitor of the Na⁺/Ca²⁺ antiporter. These observations suggest that during the sustained phase of stimulation with AII, a CBDMB-sensitive mechanism, rather than dihydropyridine-sensitive calcium channels, is involved in Ca²⁺ uptake in rat glomerulosa cells. The bulk Ca²⁺ influx did not correlate with aldosterone production; however, the maintained activity of different Ca²⁺ entry mechanisms seems to be essential for AII-induced aldosterone production.

Journal of Endocrinology (1989) 122, 361–370

This article has been cited by other articles:

				M. D. Payet, T. L. Goodfriend, L. Bilodeau, C. Mackendale, L. Chouinard, and N. Gallo-Payet An oxidized metabolite of linoleic acid increases intracellular calcium in rat adrenal glomerulosa cells Am J Physiol Endocrinol Metab, December 1, 2006; 291(6): E1160 - E1167. [Abstract] [Full Text] [PDF]

				A. SPAT and L. HUNYADY Control of Aldosterone Secretion: A Model for Convergence in Cellular Signaling Pathways Physiol Rev, April 1, 2004; 84(2): 489 - 539. [Abstract] [Full Text] [PDF]

				J. Li, R. E. Feltzer, K. L. Dawson, E. A. Hudson, and B. J. Clark Janus Kinase 2 and Calcium Are Required for Angiotensin II-dependent Activation of Steroidogenic Acute Regulatory Protein Transcription in H295R Human Adrenocortical Cells J. Biol. Chem., December 26, 2003; 278(52): 52355 - 52362. [Abstract] [Full Text] [PDF]

				J. K. Makara, P. Koncz, G. L. Petheo, and A. Spat Role of Cell Volume in K+-Induced Ca2+ Signaling by Rat Adrenal Glomerulosa Cells Endocrinology, November 1, 2003; 144(11): 4916 - 4922. [Abstract] [Full Text] [PDF]

				J. K. Makara, G. L. Petheo, A. Toth, and A. Spat Effect of Osmolarity on Aldosterone Production by Rat Adrenal Glomerulosa Cells Endocrinology, May 1, 2000; 141(5): 1705 - 1710. [Abstract] [Full Text] [PDF]

				B. J. Clark and R. Combs Angiotensin II and Cyclic Adenosine 3',5'-Monophosphate Induce Human Steroidogenic Acute Regulatory Protein Transcription through a Common Steroidogenic Factor-1 Element Endocrinology, October 1, 1999; 140(10): 4390 - 4398. [Abstract] [Full Text]

				N. Cherradi, M. F. Rossier, M. B. Vallotton, and A. M. Capponi Calcium Stimulates Intramitochondrial Cholesterol Transfer in Bovine Adrenal Glomerulosa Cells J. Biol. Chem., October 18, 1996; 271(42): 25971 - 25975. [Abstract] [Full Text] [PDF]