This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by QUINN, S. J. Articles by WILLIAMS, G. H. Search for Related Content PubMed PubMed Citation Articles by QUINN, S. J. Articles by WILLIAMS, G. H.

Kinetics of Cytosolic Calcium and Aldosterone Responses in Rat Adrenal Glomerulosa Cells^*

Department of Physiology, Boston University School of Medicine (D.L.T.) Boston, Massachusetts 02118
Department of Physiology, Semmelweis University Medical School (P.E.) Budapest, Hungary
Endocrine-Hypertension Division, Department of Medicine, Brighamand Women's Hospital, and Harvard Medical School Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Dr. Stephen J. Quinn, Endocrine-Hypertension Division, Brigham and Women’s Hospital, 221 Longwood Avenue, Boston, Massachusetts 02115.

Abstract

To evaluate the relationship between cytosolic calcium (Ca_i) and aldosterone production, rat adrenal zona glomerulosa (ZG) cells were studied during long-term stimulation by different secretagogues. Ca_i was measured in single ZG cells using microspectrofluorimetry, and aldosterone was determined in cell populations using a superfusion system. For external potassium (K⁺), Ca_i increases are sustained, with only a slight decrement over time, a feature shared by aldosterone production. The relationship between aldosterone output and Ca_i is nonlinear, with a Ca_i value for half-maximal stimulation of approximately 500 nM. Furthermore, the sustained changes in Cas with external K⁺ indicate that ZG cells can use an amplitude-based Cai signal to stimulate aldosterone production. Ca_i changes stimulated by angiotensin-II (Ang-II) show a complex doseresponse pattern, with high concentrations (1 nM) of Ang-II eliciting a peak-plateau signal and lower doses (0.1 nM to 10 pM) producing repeated Ca_i oscillations. The peak amplitude of the Ca_i response in individual cells is not dose dependent, with the ZG cell experiencing peak levels repeatedly at the lowest Ang-II concentrations. However, the Ca_i transients are more frequent with increasing Ang-II concentrations between 0.1 nM and 10 pM. When integrated over time, the mean Cai signal also shows only modest dose-dependency during the sustained phase of Ang-II stimulation. Unlike the integrated Ca_i signal, aldosterone production increases steeply between 10 pM and 0.1 nM Ang-II, indicating that the Ca_i signal is likely to be frequency-based. Conversely, the steroid response to high Ang-II closely mirrors the kinetics of the more sustained Ca_i signals, including the diminished Ca_i and aldosterone levels during sustained stimulation with the highest Ang-II doses. Arginine vasopressin stimulated Ca_i and aldosterone responses, which closely resemble those elicited by 0.1 nM Ang-II, except that both Ca_i and aldosterone return to basal values within 20 min of continuous presentation of arginine vasopressin. Each ZG secretagogue produces a distinct pattern of Ca_i and aldosterone response. In addition, Ca_i response patterns can be divided into two general classes: a sustained Ca_i response, which appears to modulate cell activation by the amplitude of the Ca_i signal, and an oscillating Ca_i response, which uses the frequency of the Ca_i transients to control the magnitude of stimulation. (Endocrinology 129: 2431–2441,1991)

Footnotes

^* This work was supported in part by grants from the NIH (DK-40127, HL-42120, and HL-42354).

Received April 9, 1991.

This article has been cited by other articles:

				J. A. Enyeart, S. J. Danthi, and J. J. Enyeart TREK-1 K+ channels couple angiotensin II receptors to membrane depolarization and aldosterone secretion in bovine adrenal glomerulosa cells Am J Physiol Endocrinol Metab, December 1, 2004; 287(6): E1154 - E1165. [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]

				M. T. Kailasam, R. J. Parmer, J. H. Cervenka, R. A. Wu, M. G. Ziegler, B. P. Kennedy, I. A. Adegbile, and D. T. O'Connor Divergent Effects of Dihydropyridine and Phenylalkylamine Calcium Channel Antagonist Classes on Autonomic Function in Human Hypertension Hypertension, July 1, 1995; 26(1): 143 - 149. [Abstract] [Full Text]