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Calcium signalling during RVD of kidney cells.

H Tinel¹, E Kinne-Saffran, R K Kinne

¹Max-Planck-Institut für molekulare Physiologie, Abteilung Epithelphysiologie, Dortmund, Germany. hanna.tinel@mpi-dortmund.mpg.de

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology

|December 23, 2000

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Kidney cells release calcium stores and allow calcium entry when swelling occurs. This calcium signaling during cell volume regulation involves arachidonic acid metabolism.

Area of Science:

Nephrology
Cell Physiology
Molecular Biology

Background:

Kidney medulla maintains high osmolarity via organic osmolytes.
Cell volume regulation under hypotonic stress involves organic osmolyte release.
This release is partially dependent on intracellular calcium levels.

Purpose of the Study:

To investigate calcium signaling mechanisms during regulatory volume decrease (RVD) in kidney cells.
To understand the role of intracellular calcium stores and extracellular calcium entry in hypotonic stress response.
To explore the involvement of arachidonic acid metabolism in this process.

Main Methods:

Utilized calcium-sensitive fluorescent dye and confocal laser scanning microscopy.
Studied primary cultures of rat inner medullary collecting duct (IMCD) cells.

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Applied hypotonic stress and various pharmacological inhibitors (ETYA, verapamil, diltiazem, nifedipine, SKF-96365).

Main Results:

Hypotonic stress triggered calcium release from intracellular stores before extracellular calcium entry in IMCD cells.
ETYA significantly reduced both the calcium response and RVD.
Voltage-dependent and receptor-mediated calcium channel blockers partially inhibited calcium influx.

Conclusions:

Swelling of IMCD cells elevates intracellular calcium through release from internal stores and influx across the cell membrane.
Arachidonic acid metabolism plays a role in the calcium signaling pathway during RVD in kidney cells.