TY - JOUR
T1 - Absence of transepithelial anion exchange by rabbit OMCD
T2 - Evidence against reversal of cell polarity
AU - Hayashi, M.
AU - Schuster, V. L.
AU - Stokes, J. B.
PY - 1988
Y1 - 1988
N2 - In the rabbit cortical collecting duct (CCD), Cl tracer crosses the epithelium predominantly via an anion exchange system that operates in either a Cl-Cl or Cl-HCO3 exchange mode. In the present study, we used the 36Cl lumen-to-bath rate coefficient (K(Cl), nm/s), a sensitive measurement of CCD transepithelial anion transport, to investigate the nature of Cl transport in the medullary collecting duct dissected from inner stripe, outer medulla (OMCD). The K(Cl) in OMCD perfused and bathed in HCO3-Ringer solution was low (46.2 ± 8.5 nm/s) and similar to that value observed in the CCD when anion exchange is inhibited and Cl permeates the epithelium by diffusion. Unlike K(Cl) in CCD, K(Cl) in OMCD was not stimulated by adenosine 3',5'-cyclic monophosphate (cAMP). OMCD K(Cl) was not altered by bath Cl and/or HCO3 removal, demonstrating the absence of transepithelial Cl-Cl and Cl-HCO3 exchange. To test the hypothesis that metabolic alkalosis could reverse the polarity of intercalated cells and thus induce an apical Cl-HCO3 exchanger in H+-secreting OMCD cells, we measured K(Cl) in OMCD from rabbits made alkalotic by deoxycorticosterone and furosemide. Although the base-line K(Cl) was slightly higher than in OMCD from control rabbits, the value was still far lower than the K(Cl) under comparable conditions in CCD. Moreover, K(Cl) in OMCD from alkalotic rabbits was unchanged by cAMP, or by sequential removal of bath HCO3 and Cl. Immunocytochemistry using peanut lectin and a monoclonal antibody to erythrocyte band 3 failed to reveal any evidence for alkalosis-induced reversal of either CCD or OMCD intercalated cell polarity. We conclude 1) Cl transport across the MCD by anion exchange is immeasurably low or nonexistent; 2) unlike the CCD, Cl transport in OMCD is not responsive to cAMP; and 3) metabolic alkalosis does not induce an apical anion exchanger in OMCD, i.e., does not cause epithelial polarity reversal.
AB - In the rabbit cortical collecting duct (CCD), Cl tracer crosses the epithelium predominantly via an anion exchange system that operates in either a Cl-Cl or Cl-HCO3 exchange mode. In the present study, we used the 36Cl lumen-to-bath rate coefficient (K(Cl), nm/s), a sensitive measurement of CCD transepithelial anion transport, to investigate the nature of Cl transport in the medullary collecting duct dissected from inner stripe, outer medulla (OMCD). The K(Cl) in OMCD perfused and bathed in HCO3-Ringer solution was low (46.2 ± 8.5 nm/s) and similar to that value observed in the CCD when anion exchange is inhibited and Cl permeates the epithelium by diffusion. Unlike K(Cl) in CCD, K(Cl) in OMCD was not stimulated by adenosine 3',5'-cyclic monophosphate (cAMP). OMCD K(Cl) was not altered by bath Cl and/or HCO3 removal, demonstrating the absence of transepithelial Cl-Cl and Cl-HCO3 exchange. To test the hypothesis that metabolic alkalosis could reverse the polarity of intercalated cells and thus induce an apical Cl-HCO3 exchanger in H+-secreting OMCD cells, we measured K(Cl) in OMCD from rabbits made alkalotic by deoxycorticosterone and furosemide. Although the base-line K(Cl) was slightly higher than in OMCD from control rabbits, the value was still far lower than the K(Cl) under comparable conditions in CCD. Moreover, K(Cl) in OMCD from alkalotic rabbits was unchanged by cAMP, or by sequential removal of bath HCO3 and Cl. Immunocytochemistry using peanut lectin and a monoclonal antibody to erythrocyte band 3 failed to reveal any evidence for alkalosis-induced reversal of either CCD or OMCD intercalated cell polarity. We conclude 1) Cl transport across the MCD by anion exchange is immeasurably low or nonexistent; 2) unlike the CCD, Cl transport in OMCD is not responsive to cAMP; and 3) metabolic alkalosis does not induce an apical anion exchanger in OMCD, i.e., does not cause epithelial polarity reversal.
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U2 - 10.1152/ajprenal.1988.255.2.f220
DO - 10.1152/ajprenal.1988.255.2.f220
M3 - Article
C2 - 3136662
AN - SCOPUS:0023813215
SN - 0002-9513
VL - 255
SP - F220-F228
JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
IS - 2 (24/2)
ER -