AJP - Renal  AJP: Regulatory, Integrative and Comparative Physiology
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Am J Physiol Renal Physiol 260: F225-F234, 1991;
0363-6127/91 $5.00
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AJP - Renal Physiology, Vol 260, Issue 2 225-F234, Copyright © 1991 by American Physiological Society


ARTICLES

Volume regulatory Cl- loss after Na+ pump inhibition in CCT principal cells

K. Strange
Children's Hospital, Division of Nephrology, Harvard Medical School, Boston, Massachusetts 02115.

Ouabain caused rabbit cortical collecting tubule (CCT) principal cells to swell 53% and then undergo regulatory volume decrease (RVD) at a rate of 4%/min to a new steady-state volume 10% below control. Reduction of peritubular Cl- concentration transiently depolarized transepithelial potential (Vte) by 36 mV and stimulated the rate of RVD 30-fold. Peritubular application of 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) inhibited RVD 74%. In contrast, luminal Cl- reduction or application of DIDS had no effect on RVD. A 10-fold elevation of perfusate K+ caused volume-regulated cells to swell 23% at a rate of 60%/min. Removal of luminal Cl- had no effect on either the rate or magnitude of K+ swelling. Peritubular or bilateral Cl- removal, however, inhibited the rate of K+ swelling by 96 and 99%, respectively. Substitution of bath Cl- for Br-, SCN-, or I- inhibited the rate of K+ swelling by 40, 38, and 98%, respectively. Surprisingly, NO3- inhibited the rate of K+ swelling by 82%. All Cl- substitutes tested transiently depolarized Vte by 3-49 mV. These results suggest strongly that RVD is mediated by a basolateral Cl- channel with a high selectivity for Cl- over other anions.





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