The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: I. Na+/H+, Cl−/HCO 3 − double exchange and Na+−Cl− symport

Cremaschi, D.; Meyer, Gerd; Rossetti, Carlo; Botta, Guido Fernando; Palestini, Paola

doi:10.1007/bf01869483

Cited by 37 publications

(27 citation statements)

References 46 publications

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“…In the previous paper (Cremaschi et al, 1987) we have shown that cellular CI-influx in the absence of bicarbonate from the bathing fluids is not affected by acetazolamide and SITS, but exhibits an immediate dependence on Na + and is inhibited by SCN-. The results presented here, concerning intracellular measurements of CI-activities, are in complete agreement.…”

Section: The Na+-ci -Symport In the Absence Of Bicarbonatementioning

confidence: 88%

“…Animals (New Zealand rabbits), preparation of gallbladder sheets and measurements of total CI uptake and of the paracellular influx (45 sec) were as described in the previous paper (Cremaschi et al, 1987).…”

Section: Methodsmentioning

confidence: 99%

“…The paracellular value used for the correction was 4.6 -+ 0.3 ~eq cm -2 hr -1 (32 exp.) and was measured as reported in the previous paper (Cremaschi et al, 1987). K + removal does not significantly affect cellular C1-influx.…”

Section: K + Removal From the Bathing Fluidsmentioning

confidence: 99%

“…The conclusion of the previous paper (Cremaschi et al, 1987) was that two Na+-C1 -entry mechanisms exist (simultaneously or alternatively) at the apical membrane of rabbit gallbladder epithelium under steady-state conditions: the first is due to a Na+/H +, CI-/HCO3 double exchange, the second to a Na +-C1-symport on a single carrier. The fact that the latter is not inhibited by furosemide even with high concentrations (10 3 M) suggests that it is not a Na +-K+-2CI -symport similar to that found in the cortical thick ascending limb of Henle's loop (Greger & Schlatter, 1981) or in the flounder intestinal epithelium (Musch et al, 1982).…”

Section: Introductionmentioning

confidence: 96%

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The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: II. Na+−Cl− symport is independent of K+

et al. 1987

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In the epithelium of rabbit gallbladder, in the nominal absence of bicarbonate, intracellular Cl- activity is about 25 mM, about 4 times higher than intracellular Cl- activity at the electrochemical equilibrium. It is essentially not affected by 10(-4) M acetazolamide and 10(-4) M 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonate (SITS) even during prolonged exposures: it falls to the equilibrium value by removal of Na+ from the lumen without significant changes of the apical membrane potential difference. Both intracellular Cl- and Na+ activities are decreased by luminal treatment with 25 mM SCN-; the initial rates of change are not significantly different. In addition, the initial rates of change of intracellular Cl- activity are not significantly different upon Na+ or Cl- entry block by the appropriate reduction of the concentration of either ion in the luminal solution. Luminal K+ removal or 10(-5) M bumetanide do not affect intracellular Cl- and Na+ activities or Cl- influx through the apical membrane. It is concluded that in the absence of bicarbonate NaCl entry is entirely due to a Na+-Cl- symport on a single carrier which, at least under the conditions tested, does not cotransport K+.

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Section: The Na+-ci -Symport In the Absence Of Bicarbonatementioning

confidence: 88%

Section: Methodsmentioning

confidence: 99%

Section: K + Removal From the Bathing Fluidsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

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The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: II. Na+−Cl− symport is independent of K+

et al. 1987

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“…Using free flow micropuncture technique in the rat, Duarte et al (34) found that during intravenous administration of furosemide sodium reabsorption in the distal tubule was not increased, even though the sodium concentration in the distal fluid was increased. It is possible that under these experimental condi- (41). However, in view of the fact that bicarbonate secretion occurs in the CCD (42)(43)(44)(45), it is more likely that the parallel antiport of Na+/H+ and Cl-/HCO-exists in the intercalated cell in the CNT.…”

Section: Methodsmentioning

confidence: 99%

Site and mechanism of action of trichlormethiazide in rabbit distal nephron segments perfused in vitro.

Shimizu¹,

Yoshitomi²,

Nakamura³

et al. 1988

J. Clin. Invest.

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To determine the exact site and mechanism of action of thiazide diuretics, effects of 104 M trichlormethiazide (TCM) on NaCJ transport were examined in the distal convoluted tubule (DCT), the connecting tubule (CNT) and the cortical collecting duct (CCD) of rabbit kidney by the in vitro microperfusion technique. TCM added to the lumen decreased lumen-to-bath 'Cl flux (JC(LB)) only in the CNT without changing the transmural voltage (VT). In the DCT, 10-4 M furosemide did not change JCI(LB) even if it was added to the lumen with 10-4 M TCM, whereas 10-5 M amiloride in the lumen decreased the lumen-to-bath 22Na flux (JNa(LB)) and VT. In the CNT, TCM added to the lumen did not affect the bath-to-lumen OC1 flux. Addition of TCM to the bath slightly decreased JC(LB). Luminal addition of 10-4 M TCM also decreased JNa(LB). Amiloride at 10-5 M in the lumen decreased both JNa(LB) and VT.Addition of TCM with 10-5 M amiloride further decreased JNa(LB) without affecting VT, indicating that TCM affects the electroneutral Na+ transport, which is distinct from the amiloride-sensitive conductive Na' pathway. When Na+ was removed from the lumen, JCI(LB) was markedly decreased, but addition of TCM did not cause further decrease in JCI(LB). Furosemide did not affect JC(LB), but addition of both 10-4 M TCM and furosemide decreased JCI(LB), indicating that Na+-K+-2CI-cotransport is not involved in the action of TCM.Removal of HCO3 slightly decreased JCI(LB), and TCM caused further decrease in JCI(LB). Amiloride at 10-3 M, a concentration supposed to inhibit the Na+/H+ antiport, slightly decreased JCI(LB), and addition of TCM caused a further marked decrease in JJI(LB). The similar results were also obtained when the combined effects of 10-3 M 4,4'-diisothiocyano-stilben-2,2'-disulfonate(DIDS) and 10'-M TCM were examined.These findings suggest that the parallel antiport of Na+/H+ and Cl-/HCO-is not involved in the action of TCM. By excluding other possible mechanisms involving neutral Na+-dependent Cl-transport, we conclude that TCM inhibits Na+-ClI cotransport in the luminal membrane of the rabbit CNT. IntroduptionAlthough thiazide diuretics have been widely used in the treatment of edema and hypertension for many years, the exact Address reprint requests to Dr. Imai,

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Epithelial Transport

Reuss

1997

Comprehensive Physiology

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The sections in this article are: Transporting Epithelia Are Sheets of Polar Cells Epithelial Structure Involves Specialized Cell–Cell and Cell–Matrix Junctions Epithelial Polarity Is Essential for Vectorial Transport Transporting Epithelia Generate and Maintain Differences in Chemical Composition Between Fluid Compartments Transepithelial Transport Involves Active Ion Transport Passive Transport Processes also Contribute to Transepithelial Transport Transepithelial Transport Involves Transcellular and Paracellular Pathways Chemical and Electrical Gradients Couple Ion Fluxes in Epithelia The Building Blocks of Epithelial Function Are Membrane Transporters Mechanisms of Ion Transport The Two‐Membrane Hypothesis: A General Epithelial‐Transport Model Mechanisms of Transepithelial NaCl Transport in Absorptive Epithelia Mechanisms of Ion Transport in Primary Cl − ‐Transporting Epithelia Mechanisms of Ion Transport in H + — and ‐Transporting Epithelia Mechanisms of Transepithelial Water Transport Transepithelial Water Transport Is Linked to Transepithelial Salt Transport Epithelia Are Widely Diverse in Their Water‐Transport Characteristics Transepithelial Water Transport in Leaky Epithelia Is Nearly Isosmotic Transepithelial Water Transport in Leaky Epithelia Can Be Transcellular and/or Paracellular Water Permeation across Cell Membranes of Some Leaky Epithelia Is via Constitutive Pores Mechanisms of Transepithelial Water Transport in ADH ‐Sensitive Epithelia Molecular Identity of Water Pores in Epithelial‐Cell Membranes Mechanisms of Regulation of Transepithelial Transport Rapid Regulation Long‐term Regulation Intramembrane Regulation and Cross‐Talk Mechanisms

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The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: I. Na+/H+, Cl−/HCO 3 − double exchange and Na+−Cl− symport

Cited by 37 publications

References 46 publications

The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: II. Na+−Cl− symport is independent of K+

The nature of the neutral Na+−Cl−-coupled entry at the apical membrane of rabbit gallbladder epithelium: II. Na+−Cl− symport is independent of K+

Site and mechanism of action of trichlormethiazide in rabbit distal nephron segments perfused in vitro.

Epithelial Transport

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