Chloride reabsorption by renal proximal tubules of necturus

A bstract. The electrical nature of active NaCl transport and the significance of a basolateral membrane chloride conductance were examined in isolated perfused rabbit proximal convoluted tubules (PCT). PCT were perfused with a high chloride solution that simulated late proximal tubular fluid and were bathed in an albumin solution that simulated rabbit serum in the control and recovery periods. The electrical nature of NaCl transport was examined by bathing the tubules in a high chloride albumin solution where there were no anion gradients.Volume reabsorption (J,) during the control and recovery period was 0.56 and 0.51 nl/mm. min, respectively, and 0.45 nl/mm -min when the tubules were bathed in a high chloride bath. The transepithelial potential difference (PD) during the control and recovery periods averaged 2.3 mV, but decreased to 0.0 mV in the absence ofanion gradients, which indicated that NaCl transport is electroneutral. Further evidence that NaCl transport is electroneutral was obtained by examining the effect of addition of 0.01 mM ouabain in PCT perfused and bathed with high chloride solutions. The J, was 0.54 nl/mm * min in the control period and not statistically different from zero after inhibition of active transport. The PD was not different from zero in both periods.Two groups of studies examined the role of basolateral membrane CF-conductance in NaCl transport. First, depolarizing the basolateral membrane with 2 mM bath Ba++ did not significantly affect J, or PD. Second, the effect of the presumptive CF-conductance inhibitor anthracene-9-CO2H was examined. Anthracene-9-CO2H did not significantly affect Jv or PD. In conclusion, these data Receivedforpublication 20 December 1983 and in revisedform 5 March 1984. show that NaCl transport in the PCT is electroneutral and transcellular and provide evidence against a significant role for basolateral membrane chloride conductance in the rabbit PCT.

Section: Resultsmentioning

confidence: 99%

Evidence for neutral transcellular NaCl transport and neutral basolateral chloride exit in the rabbit proximal convoluted tubule.

Baum

Berry

1984

“…Solute uptake was assayed by a rapid filtration technique (43). The usual composition of the final incubation media was 40 mM K2SO4, 20 mM Na36Cl or 20 mM tetramethyl-ammonium (TMA)36CI (9.5 !Ci/ml), 0.14 mM _[3H]glucose (22 (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18), possible conductive entry of Na+ [30,50], neutral, coupled entry with chloride [28,[51][52][53][54][55][56][57], and Na+/H+ exchange [30,58]). Therefore, to simplify the study of 36CL-uptake, Na+ was replaced by another cation, TMA+, which we assume to be impermeant (28,55).…”

Section: Methodsmentioning

confidence: 99%

“…Other workers have proposed that sodium chloride is transported across the luminal membrane of the proximal tubule, intestine, rectal gland, and gallbladder as an electrically neutral ternary complex (28,(51)(52)(53)(54)(55)(56)(57). It is possible that this additional form of transport couples chloride entry to the sodium gradient across the luminal membrane of the proximal tubule.…”

Section: Methodsmentioning

confidence: 99%

“…Several investigators (19)(20)(21)(22)(23)(24)(25) have proposed that "passive" paracellular transport mechanisms (e.g., diffusion, convection) may contribute to the reabsorption ofsalt and water in the late proximal tubule (19)(20)(21)(22)(23)(24)(25). Alternatively, recent studies suggest that transcellular, electrically neutral transport of chloride may occur in the late proximal tubule (26)(27)(28)(29). A specific model for neutral NaCl reabsorption has been proposed for the proximal tubule that incorporates a parallel arrangement of Na+/H+ and C1-/0H-exchange mechanisms in the luminal membrane (29).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Chloride Uptake by Brush Border Membrane Vesicles Isolated from Rabbit Renal Cortex

Warnock¹,

Yee²

1981

112

A B S T R A C T Brush border membrane vesicles were isolated from rabbit renal cortex by Mg++-precipitation and differential centrifugation. NCI-and [3H]glucose uptakes were simultaneously determined by a rapid filtration technique. Lysis of the vesicles with distilled water abolished 90-95% of the radioactivity on the filters, suggesting that nearly all of the 36Cl-and [3H]-glucose counts represented uptake into an osmotically reactive intravesicular space. Inwardly directed K+ gradients plus valinomycin stimulated 36C1-uptake, demonstrating a conductive pathway for chloride uptake into brush-border membrane vesicles. 36C-uptake could also be stimulated by inwardly directed proton gradients (pHoutside < pHinside). This effect was seen in the absence of sodium, as well as in the presence of valinomycin when the vesicles had equal K+ concentrations inside and out. An "overshoot" phenomenon was observed when external 36C-was 2 mM and the external pH was lowered from 7.5 to 6.0 or to 4.5. The effect of the proton gradient was presumed to be different from the conductive mechanism because (a ) the stimulation of3Cl-uptake by inwardly directed K+ diffusion potentials was additive to the proton gradient effect, and (b) competition studies revealed statistically significant effects of thiocyanate on the conductive pathway, but not on the proton-driven pathway.HC1 cotransport or anion exchange are electrically neutral mechanisms which could couple 3Cl-uptake to inwardly-directed proton gradients in a brush border Portions of these results were presented at the 64th Annual

“…This process fundamentally relies on active sodium transport, and has been considered for the gut, gall bladder, and proximal tubule (11)(12)(13)(14)(15)(16)(17)(18)(19). These models presume that the route of neutral sodium chloride reabsorption is through the cells of the transporting epithelium, and specify that chloride entry cannot be accounted for by the electrochemical potential gradient for chloride across the luminal membrane.…”

mentioning

confidence: 99%

Effects of Anion-Transport Inhibitors on NaCl Reabsorption in the Rat Superficial Proximal Convoluted Tubule

Lucci¹,

Warnock²

1979

A B S T R A C T The effects of anion-transport inhibitors on volume reabsorption, and total CO2 concentrations were examined by in vivo microperfusion of superficial proximal convoluted tubules of rats. The luminal perfusion solution was a high-chloride, lowbicarbonate solution like that in the in vivo late proximal tubule. The anion-transport inhibitors were only added to the luminal perfusion solutions.In tubules perfused with the control high-chloride solution, the rate of volume reabsorption (J,) was 2.3±0.2 nl/mm min (n = 18), and the collected total CO2 concentration was 4.0±0.3 mM. Furosemide (3 mM) caused a marked reduction in volume reabsorption to 0.8±0.3 nl/mmmin (n = 20) and only a slight increase in the total CO2 concentration of collected samples of perfusate (7.8±0.5 mM). 0.8 mM acetazolamide caused a more pronounced rise in the collected total CO2 concentrations to 10.7±0.5 mM but only a slight fall in J, to 1.7±0.3 nl/mm-min (n = 19). Hence, we inferred that inhibition of carbonic anhydrase only partially accounted for the inhibition of J, by furosemide. 4-acetamido-4'-iso-thiocyanato-stilbene-2,2'-disulphonic acid (0.1 mM), a well-characterized inhibitor of erythrocyte anion exchange mechanisms, also reduced J, to 1.6±0.3 nl/mm min (n = 15) without changing the total CO2 concentrations of the collected perfusates (3.6±0.4 mM). The effect of 4-acetamidoA4'-iso-thiocyanato-stilbene-2,2'-disulphonicPortions of this work were presented at the 10th Annual