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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 4,4â-diisothiocyanostilbene-2,2â-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 Kâ 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
AJP - Renal Physiology – The American Physiological Society
Published: Feb 1, 1991
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