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Am J Physiol Renal Physiol 275: F198-F203, 1998;
0363-6127/98 $5.00
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Vol. 275, Issue 2, F198-F203, August 1998

Extracellular Ca2+ decreases chloride reabsorption in rat CTAL by inhibiting cAMP pathway

Marie Céleste De Jesus Ferreira and Claire Bailly

Unité de Recherche Associée Centre National de la Recherche Scientifique 1859, Département de Biologie Cellulaire et Moléculaire, Commissariat à l'Énergie Atomique-Saclay, 91191 Gif-sur-Yvette, France

The effect of activation of the Ca2+-sensing receptor on net Cl flux (JCl) has been investigated on microperfused cortical (C) thick ascending limb (TAL) from rat kidney. Increasing bath Ca2+ from 0.5 to 3 mM or adding 200 µM of the specific Ca2+-sensing receptor agonist neomycin reduced basal as well as antidiuretic hormone (ADH)-stimulated JCl by 27.7 ± 5.0% and 25.9 ± 4.1%, respectively. JCl remained unchanged in time control tubules. The effect of neomycin/Ca2+ on JCl was blocked by two protein kinase A inhibitors, H-9 or H-89, but not by a protein kinase C inhibitor, GF-109203X, regardless of whether ADH was present or not. Moreover, H-89 decreased basal JCl and prevented a further effect of 3 mM Ca2+. When JCl was increased by 8-bromo-cAMP plus IBMX, no effect of 3 mM Ca2+ was observed. Inhibitors of phospholipase A2 and cytochrome P-450 monooxygenase failed to modify the effect of 3 mM Ca2+, although these agents dampened significantly the inhibitory effect of bradykinin on medullary TAL. We conclude that extracellular Ca2+ decreases basal and ADH-stimulated Cl reabsorption in CTAL by inhibiting the cAMP pathway, independently of protein kinase C or phospholipase A2 stimulation.

calcium; in vitro microperfusion; protein kinases


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