Evidence for electroneutral chloride transport in rabbit renal cortical brush border membrane vesicles

Shiuan, David; Weinstein, S. W.

doi:10.1152/ajprenal.1984.247.5.f837

Cited by 13 publications

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“…There have been previous proposals for the existence of Cl--OH-exchange in cell membranes. These have been specifically for epithelial membranes, and are based solely on radiolabelled Cl-flux studies in vesicles prepared from brush-border membranes of rabbit renal cortex (Shiuan & Weinstein, 1984) and rabbit ileum (Fan, Faust & Powell, 1983), and from apical membranes of rat distal colon (Rajendran & Binder, 1993). Interestingly, this last report suggests the co-existence of an AE and a CHE carrier, although there is no evidence for the effect of these carriers on pH,.…”

Section: Discussionmentioning

confidence: 99%

Novel chloride‐dependent acid loader in the guinea‐pig ventricular myocyte: part of a dual acid‐loading mechanism.

Sun

Leem

Vaughan‐Jones

1996

The Journal of Physiology

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1. The fall of intracellular pH (pHi) following the reduction of extracellular pH (pH.) was investigated in guinea-pig isolated ventricular myocytes using intracellular fluorescence measurements of carboxy-SNARF-1 (to monitor pH,). Cell superfusates were buffered either with a 5% CO2-HCO3 system or were nominally C02-HC03-free.2. Reduction of pHo from 7A4 to 6A4 reversibly reduced pHi by about 0 4 pH units, independent of the buffer system used.3. In HC03--free conditions, acid loading in low pHo was not dependent on Na`-H+ exchange or on the presence of Na+. It was unaffected by high-K+ solution, by voltage-clamp depolarization, by various divalent cations (Zn2+, Cd2+, Ni2+ and Ba2P) and by the organic Ca2+ channel blocker diltiazem, thus ruling out proton influx through H+-or Ca2+-conductance channels or influx via a K+-H+ exchanger. The fall also persisted in the presence of glycolytic inhibitors, or the lactate transport inhibitor, a-cyano-4-hydroxy cinnamate.4. In HC03--free conditions, acid loading in low pH0 was reversibly inhibited (by up to 85 %) by Cl-removal and was slowed by the stilbene drug DBDS (dibenzamidostilbene disulphonic acid). In contrast, the Cl--HCO3 exchange inhibitor DIDS (4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid) had no inhibitory effect. Acid loading is therefore mediated by a novel CF-dependent, acid influx pathway. 5. After switching to C02-HC03--buffered conditions, acid loading was doubled. It was still not inhibited by Nae-free or high-K+ solutions but was once again inhibited (by 78 %) in Clfree solution. The HC03--stimulated fraction of acid loading was inhibited by DIDS. 6. We propose a model of acid loading in the cardiomyocyte which consists of two parallel carriers. One is Cl--HCO3-exchange, while we suggest the other to be a novel ClF-OHexchanger (although we do not rule out the alternative configuration of H+-Cl-co-influx). The proposed dual acid-loading mechanism accounts for most of the sensitivity of pHi to a fall of pHo.Intracellular pH is an important physiological modulator of cardiac contraction (see Orchard & Kentish, 1990 for review). This is largely because reducing pH, reduces Ca2+ binding to troponin-C, thereby attenuating the force of contraction. Of the many conditions that can reduce pHi in cardiac cells, a common one is a reduction of extracellular pH. Over the physiological range of pH, intracellular pH is related approximately linearly to pH., with a transfer function (slope of pH1 vs. pHO) of 0 3-0'4 (Ellis & Thomas, 1976;Vaughan-Jones, 1986). Thus, because extracellular pH is an important modulator of pHi in cardiac cells, it becomes an important modulator of contractility in the heart. The mechaWism, however, whereby pHi is linked to pH0 remains unknown (Sun & Vaughan-Jones, 1994). This is the case not only for cardiac cells, but also for many other cell types. In the present work, we have investigated the mechanism linking pHi to pH0 in single enzymically isolated cardiomyocytes, while measuring pH1 using the pH-sensitive fluorophore, ...

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Section: Discussionmentioning

confidence: 99%

Novel chloride‐dependent acid loader in the guinea‐pig ventricular myocyte: part of a dual acid‐loading mechanism.

Sun

Leem

Vaughan‐Jones

1996

The Journal of Physiology

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“…Subsequent studies in isolated apical membrane vesicles have disagreed with respect to the presence or absence of C1/OH exchange (9)(10)(11)(12)(13)(14)(15). Karniski and Aronson (16) found rapid Cl/formate exchange in these apical membranes.…”

Section: Introductionmentioning

confidence: 99%

Apical membrane chloride/base exchange in the rat proximal convoluted tubule.

Alpern¹

1987

J. Clin. Invest.

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To examine whether Cl/base exchange is present on the apical membrane of the proximal convoluted tubule, cell pH was measured fluorometrically in the in vivo microperfused rat proximal tubule with (2',7')-bis(carboxyethyl)-(5,6)-carboxyfluorescein.The effect of luminal chloride addition was examined in tubules perfused symmetrically with chloride-free solutions. In the absence of inhibitors, luminal chloride addition did not affect cell pH. However, after inhibition of basolateral membrane anion transport with peritubular 4-acetamido-4'-isothiocyano-(2,2')-disulfonic-stilbene (to amplify effects of apical membrane transport on cell pH), luminal chloride addition caused a small cell acidification (delta pH, = 0.02). When 1 mM formate was added to the solutions, luminal chloride addition caused a larger change in cell pH (delta pH, = 0.06) that was inhibited by (4,4')-diisothiocyano-(2,2')-disulfonic-stilbene. This stimulation of Cl/base exchange was not seen with 1 mM acetate addition. These results demonstrate apical membrane Cl/base exchange, a significant fraction of which is dependent on the presence of formate and probably represents Cl/formate exchange.

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“…Warnock and Yee (2) first demonstrated an electroneutral Cl-/base exchanger in brush border vesicles. Subsequent vesicle studies either confirmed (3)(4)(5) or failed to obtain (6-9) similar results. In contrast to the apical membrane, the presence of Na+-independent Cl-/base exchange in basolateral membrane vesicles (10)(11)(12) and whole tubule studies (13)(14)(15)(16)(17) is less controversial.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of apical and basolateral Na(+)-independent Cl-/base exchange in the rabbit superficial proximal straight tubule.

Kurtz

Nagami²,

Yanagawa³

et al. 1994

J. Clin. Invest.

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The present study was undertaken to determine the magnitude and mechanism of base transport via the apical and basolateral Na '-independent Cl -/base exchangers in rabbit isolated perfused superficial S2 proximal tubules. The results demonstrate that there is an apical Na '-independent Cl-/ base exchanger on both membranes. HCO3 fails to stimulate apical Cl-/base exchange in contrast to the basolateral exchanger. Inhibition of endogenous HCO3 production does not alter the rate of apical Cl-/base exchange in Hepesbuffered solutions. Both exchangers are inhibited by H2DIDS and furosemide; however, the basolateral anion exchanger is more sensitive to these inhibitors. The results indicate that the apical and basolateral Cl-/base exchangers differ in their transport properties and are able to transport base equivalents in the absence of formate. The formate concentration in rabbit arterial serum is -6 ,uM and in vitro tubule formate production is < 0.6 pmol/min per mm.Formate in the micromolar range stimulates Jv in a dosedependent manner in the absence of a transepithelial Na+ and Cl-gradient and without a measurable effect on Cl--induced equivalent base flux. Apical formic acid recycling cannot be an important component of any cell model, which accounts for formic acid stimulation of transcellular NaCl transport in the rabbit superficial S2 proximal tubule. We propose that transcellular NaCl transport in this nephron segment is mediated by an apical Na+/H+ exchanger in parallel with a Cl-/OH-exchanger and that the secreted H+ and OH -ions form H20 in the tubule lumen. (J. Clin. Invest. 1994. 94:173-183.) Key words: Na+/H+ exchange-

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Evidence for electroneutral chloride transport in rabbit renal cortical brush border membrane vesicles

Cited by 13 publications

References 0 publications

Novel chloride‐dependent acid loader in the guinea‐pig ventricular myocyte: part of a dual acid‐loading mechanism.

Novel chloride‐dependent acid loader in the guinea‐pig ventricular myocyte: part of a dual acid‐loading mechanism.

Apical membrane chloride/base exchange in the rat proximal convoluted tubule.

Mechanism of apical and basolateral Na(+)-independent Cl-/base exchange in the rabbit superficial proximal straight tubule.

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