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

Volume regulatory Cl- loss after Na+ pump inhibition in CCT principal cells Hospital, Division of Nephrology, Harvard Medical School, Boston, Massachusetts STRANGE, KEV. regulatory Cl- loss after Na+ pump CCT . Am. J. Physiol. 260 (Renal Fluid Electrolyte Physiol. 29): F225-F234, 1991.-Ouaba causedrabbit cortical collectg tubule (CCT) to swell53% and then undergoregulatory decrease (RVD) at a rate of 4%/m to a new steady-state 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’-disulfonicacid (DIDS) hibited RVD 74%. contrast, lumal Cl- reduction or application of DIDS had no effect on RVD. A lo-fold elevation of perfusate K+ caused-regulated to swell 23% at a rate of 60%/m. Removal of lumal Cl- had no effect on either the rate or magnitude of K+ swellg. Peritubular or bilateral Cl- removal, however, hibited the rate of K+ swellg by 96 and 99%, respectively. Substitution of bath Cl- for Br-, SCN-, or I- hibited the rate of K+ swellg by 40, 38, and 98%, respectively. Surprisgly, NO; hibited the rate of K’ swellgby 82%. All Cl- substitutestested transiently depolarized Vte by 3-49 mV. These results suggeststrongly that RVD is mediatedby a basolateralCl- channel with a high http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Renal Physiology The American Physiological Society

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

AJP - Renal Physiology , Volume 260: F225 – Feb 1, 1991

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Publisher
The American Physiological Society
Copyright
Copyright © 1991 the American Physiological Society
ISSN
0363-6127
eISSN
1522-1466
Publisher site
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Abstract

Hospital, Division of Nephrology, Harvard Medical School, Boston, Massachusetts STRANGE, KEV. regulatory Cl- loss after Na+ pump CCT . Am. J. Physiol. 260 (Renal Fluid Electrolyte Physiol. 29): F225-F234, 1991.-Ouaba causedrabbit cortical collectg tubule (CCT) to swell53% and then undergoregulatory decrease (RVD) at a rate of 4%/m to a new steady-state 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’-disulfonicacid (DIDS) hibited RVD 74%. contrast, lumal Cl- reduction or application of DIDS had no effect on RVD. A lo-fold elevation of perfusate K+ caused-regulated to swell 23% at a rate of 60%/m. Removal of lumal Cl- had no effect on either the rate or magnitude of K+ swellg. Peritubular or bilateral Cl- removal, however, hibited the rate of K+ swellg by 96 and 99%, respectively. Substitution of bath Cl- for Br-, SCN-, or I- hibited the rate of K+ swellg by 40, 38, and 98%, respectively. Surprisgly, NO; hibited the rate of K’ swellgby 82%. All Cl- substitutestested transiently depolarized Vte by 3-49 mV. These results suggeststrongly that RVD is mediatedby a basolateralCl- channel with a high

Journal

AJP - Renal PhysiologyThe American Physiological Society

Published: Feb 1, 1991

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