This Article Full Text Full Text (PDF) All Versions of this Article: 144/11/4916    most recent Author Manuscript (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map 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 Makara, J. K. Articles by Spät, A. Search for Related Content PubMed PubMed Citation Articles by Makara, J. K. Articles by Spät, A.

Role of Cell Volume in K⁺-Induced Ca²⁺ Signaling by Rat Adrenal Glomerulosa Cells

Department of Physiology and Laboratory of Cellular and Molecular Physiology, Semmelweis University Medical School and Hungarian Academy of Sciences, H-1444 Budapest, Hungary

Address all correspondence and requests for reprints to: Prof. A. Spät, Department of Physiology, Semmelweis University Medical School, P.O. Box 259, H-1444 Budapest, Hungary. E-mail: Spat{at}Puskin.SOTE.Hu.

The involvement of cell volume in the K⁺-evoked Ca²⁺ signaling was studied in cultured rat glomerulosa cells. Previously we reported that hyposmosis (250 mOsm) increased the amplitude of T-type Ca²⁺ current and, accordingly, enhanced the Ca²⁺ response of cultured rat glomerulosa cells to K⁺. In the present study we found that this enhancement is not influenced by the cytoskeleton-disrupting drugs cytochalasin-D (20 µM) and colchicine (100 µM). Elevation of extracellular potassium concentration ([K⁺]_e) from 3.6 to 4.6–8.6 mM induced cell swelling, which had slower kinetics than the Ca²⁺ signal. Cytoplasmic Ca²⁺ signal measured in single glomerulosa cells in response to stimulation with 5 mM K⁺ for 2 min showed two phases: after a rapid rise reaching a plateau within 20–30 sec, [Ca²⁺]_c increased further slowly by approximately one third. When 5 mM K⁺ was coapplied with elevation of extracellular osmolarity from 290 to 320 mOsm, the second phase was prevented. These results indicate that cell swelling evoked by physiological elevation of [K⁺]_e may contribute to the generation of sustained Ca²⁺ signals by enhancing voltage-activated Ca²⁺ influx.

This article has been cited by other articles:

				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]