Role of Cl− in Electrogenic H+ Secretion by Cortical Distal Tubule

Role of Cl− in Electrogenic H+ Secretion by Cortical Distal Tubule The presence of an electrogenic H+-ATPase has been described in the late distal tubule, a segment which contains intercalated cells. The present paper studies the electrogenicity of this transport mechanism, which has been demonstrated in turtle bladder and in cortical collecting duct. Transepithelial PD (V t ) was measured by means of Ling-Gerard microelectrodes in late distal tubule of rat renal cortex during in vivo microperfusion. The tubules were perfused with electrolyte solutions to which 2 × 10−7 m bafilomycin or 4.6 × 10−8 m concanamycin were added. No significant increase in lumen-negative V t upon perfusion with these inhibitors as compared to control, was observed as well as when 10−3 m amiloride, 10−5 m benzamil or 3 mm Ba2+ were perfused alone or in combination. The effect of an inhibition of electrogenic H+ secretion, i.e., increase in lumen-negative V t by 2–4 mV, was observed only when Cl− channels were blocked by 10−5 m 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB). This blocker also reduced the rate of bicarbonate reabsorption in this segment from 1.21 ± 0.14 (n= 8) to 0.62 ± 0.03 (8) nmol.cm−2.sec−1 as determined by stationary microperfusion and pH measurement by ion-exchange resin microelectrodes. These results indicate that: (i) the participation of the vacuolar H+ ATPase in the establishment of cortical late distal tubule V t is minor in physiological conditions, but can be demonstrated after blocking Cl− channels, thus suggesting a shunting effect of this anion; and, (ii) the rate of H+ secretion in this segment is reduced by a Cl− channel blocker, supporting coupling of H+-ATPase with Cl− transport. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Membrane Biology Springer Journals

Role of Cl− in Electrogenic H+ Secretion by Cortical Distal Tubule

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Publisher
Springer-Verlag
Copyright
Copyright © Inc. by 1997 Springer-Verlag New York
Subject
Life Sciences; Biochemistry, general; Human Physiology
ISSN
0022-2631
eISSN
1432-1424
D.O.I.
10.1007/s002329900228
Publisher site
See Article on Publisher Site

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