Role of calcium fluxes in the sustained phase of angiotensin II-mediated aldosterone secretion from adrenal glomerulosa cells.

Kojima, I; Kojima, K; Rasmussen, H

doi:10.1016/s0021-9258(17)39349-3

Cited by 142Hormonal Regulation and HypertensionRenin-Angiotensin System StudiesIon channel regulation and function

Role of calcium fluxes in the sustained phase of angiotensin II-mediated aldosterone secretion from adrenal glomerulosa cells.

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Kojima, I, Kojima, K, Rasmussen, H·1985·Journal of Biological Chemistry

DOI 10.1016/s0021-9258(17)39349-3

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Abstract

When angiotensin II stimulates aldosterone secretion, it causes a rapid but transient mobilization of calcium from an intracellular pool and a sustained increase in the influx of calcium in adrenal glomerulosa cells. The present studies were undertaken to determine the respective roles of the two angiotensin II-induced changes in cellular calcium metabolism in modulating events during the sustained phase of cellular response which is thought to be mediated by the C-kinase branch of the calcium messenger system. The sustained response to angiotensin II is only 50% of maximal in cells pretreated with dantrolene in a concentration sufficient to inhibit the angiotensin II-induced mobilization of intracellular calcium. Also, if A23187 is added to cells simultaneously with 1-oleoyl-2-acetylglycerol (OAG), the aldosterone secretory response is similar to that seen after angiotensin II. However, if A23187 is added first and the transient aldosterone secretory response allowed to decay, and OAG then added, the sustained aldosterone secretory response is only 45-50% of maximal. Addition of the calcium channel agonist, BAY K 8644, with OAG leads to an aldosterone secretory response which is only 50% of maximal, but if upon addition of OAG and BAY K 8644 the cells are also exposed for 5 min to media containing 8 mM K+, then the sustained secretory response is maximal. These data imply that the initial transient rise in the [Ca2+] of the cell cytosol plays a role in determining the extent to which C-kinase is shifted from its calcium-insensitive to its calcium-sensitive form. The second group of experiments examined the relationship between the sustained angiotensin II-induced increase in plasma membrane calcium influx and the sustained aldosterone secretory response. The results show that in the presence of 1 microM nitrendipine or 2 mM extracellular K+, angiotensin II causes no increase in calcium influx and only a transient rather than a sustained increase in the rate of aldosterone secretion indicating that the sustained phase of the response is dependent upon a continued high rate of Ca2+ influx which regulates the rate of turnover of the activated C-kinase.

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Extremely low potassium levels (2 mmol/l) actually reduce aldosterone production stimulated by angiotensin II, but do not stop it completely.
“Extremely low potassium levels (2 mmol/l) actually reduce aldosterone production stimulated by angiotensin II, but does not stop it completely (Kojima et al., 1985; Chen et al., 1999).”
From Thoroughly Calibrated Modular Agent-Based Model of the Human Cardiovascular and Renal Systems for Blood Pressure Regulation in Health and Disease (2021) · cites this paper as Kojima et al., 1985

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Authors: Kojima, I., Kojima, K., & Rasmussen, H.
Affiliations: Yale University (US)
ORCID: Kojima, I
Rasmussen, H
Venue: Journal of Biological Chemistry
Publisher: Elsevier BV
Published: 1985-08
Volume: 260
Issue: 16
Pages: 9177-9184
ISSN: 0021-9258 (ISSN-L)
DOI: 10.1016/s0021-9258(17)39349-3
OpenAlex: W1546020694
Cited by: 142
References: 29
Citations by year: 2023: 2 · 2021: 1 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 2 · 2014: 2
FWCI: 17.53
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by/4.0/ (vor, 12875 d)
Locations: Journal of Biological Chemistry (publishedVersion, cc-by)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r01am019813-10)
Topics: Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
Keywords: angiotensin II, aldosterone secretion, adrenal glomerulosa cells, calcium flux, calcium mobilization, protein kinase C, dantrolene, 1-oleoyl-2-acetylglycerol, Bay K 8644, nitrendipine, extracellular potassium
MeSH terms: Calcimycin, Adrenal Glands, Aldosterone, Angiotensin II, Animals, 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester, Calcium, Calcium Channel Blockers, Cattle, Dantrolene, Ion Channels, Kinetics, Models, Biological, Nifedipine, Nitrendipine, Potassium, In Vitro Techniques

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Role of calcium fluxes in the sustained phase of angiotensin II-mediated aldosterone secretion from adrenal glomerulosa cells.

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