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PubMed1992

Functions of ascending thin limb of Henle's loop with special emphasis on mechanism of NaCl transport.

Major controversy concerning the ascending thin limb of Henle's loop (ATL) centers on the urine concentration mechanism based on the countercurrent multiplier system in the inner medulla of the kidney. This renal tubular segment has specific transport properties which function to dilute the urine without any movement of water across the epithelium. This segment is fundamentally impermeable to water, moderately permeable to urea, and highly permeable to Na+ and Cl-. Whether NaCl is reabsorbed actively in the ATL has long been an important question. While mathematical modelling studies have failed to explain completely how the osmotic gradient in the inner medulla is generated without active NaCl transport in the ATL, the experimental data support the view that active NaCl reabsorption is absent. Recently, we succeeded in measuring the intracellular Na+ concentration by using the fluorescent Na+ indicator sodium-binding benzofuran isophthalate in the in vitro microperfused ATL. Our data suggest that the ATL maintains a low intracellular Na+ concentration by the ouabain-sensitive Na+/K+ ATPase in the basolateral membrane, and that the luminal membrane of the ATL has furosemide-insensitive Na+ permeability. Active Na+ reabsorption estimated in our study amounts to only a few per cents of the net Na+ reabsorption in the ATL. It is therefore suggested that the major role of Na+ extrusion in the ATL cells is to maintain a low cellular Na+ concentration against ambient hyperosmolarity, although small but substantial amount of Na+ is reabsorbed by the furosemide-insensitive Na+ permeability and ouabain-sensitive Na+/K+ ATPase.

Animals↗
PubMed1991

Selectivity of ion permeability across ascending thin limb of Henle's loop: interaction of Cl- and other halogens with anion transport system.

In hamster ascending thin limb of Henle's loop (ATL) perfused in vitro, we examined halogen selective permeability and effects on Cl- transport. Relative permeabilities for halogens to sodium (PX/PNa) were determined by single salt dilution voltage. (PF/PNA, PCl/PNa, PBr/PNa and PI/PNa were 0.47 +/- 0.09, 3.23 +/- 0.22, 3.23 +/- 0.26, and 0.47 +/- 0.09, respectively. Simultaneous determination of 36Cl and 125I fluxes confirmed that addition of 10(-4) M 5-nitro-2-(3-phenyl-propylamino)-benzoate (NPPB), a Cl- channel blocker, to the bath decreased the flux coefficient for 36Cl (10(-7) cm2/s) from 67.0 +/- 11.7 to 29.5 +/- 7.9 without affecting that for 125I. NPPB also reduced both PCl/PNa and PBr/PNa from 2.67 +/- 0.20 to 0.95 +/- 0.12 and from 2.33 +/- 0.24 to 1.32 +/- 0.12, respectively. Addition of 100 mM Cl- or I- decreased 36Cl flux coefficient from 124.8 +/- 14.3 to 87.7 +/- 13.0 or to 41.0 +/- 11.6 without affecting that for 125I. All other halogens and SCN- also exhibited inhibitory effects on 36Cl flux. These findings support the hypothesis that the putative Cl- channel in the ATL is highly permeable to both Cl- and Br- but less permeable to I-, F-, and SCN-. They suggest that there are at least two functionally distinct components in the process of Cl- transport across the ATL, the binding site and the selective barrier. All halogens may compete against Cl- at the binding site.

Animals↗
PubMed1983

Chloride transport in the thick ascending limb of Henle's loop: potassium dependence and stoichiometry of the NaCl cotransport system in plasma membrane vesicles.

Cells were isolated from the thick ascending limb of Henle's loop of rabbit kidney outer medulla and a plasma membrane fraction was prepared by differential centrifugation. Sodium and rubidium uptake into the plasma membrane vesicles were determined by a rapid filtration technique. In the presence of a 100 mM KCl gradient and 0.5 mM sodium the vesicles took up 252 +/- 82 pmoles sodium/mg protein X 15s; 52% of the uptake was dependent on the presence of chloride or inhibited by 10(-3) M bumetanide. If KCl was stepwise replaced by choline chloride, sodium uptake decreased in the absence of bumetanide but was only insignificantly altered in the presence of bumetanide. Potassium exerted a halfmaximum stimulation at 22.3 +/- 9.7 mM. In tracer exchange experiments under zero salt gradient conditions, sodium uptake was also strongly reduced in the absence of potassium. Rubidium uptake into the same membrane fraction was highest in the presence of a NaCl gradient, and decreased 41% when sodium was replaced by choline or when 10(-3) M bumetanide was present. Replacement of sodium chloride by sodium nitrate also inhibited rubidium uptake. When the sodium, chloride and potassium dependence of the bumetanide sensitive sodium uptake was investigated in more detail, Hill coefficients for sodium of 1.0 +/- 0.03, for chloride of 1.8 +/- 0.2 and for potassium of 0.98 +/- 0.03 were obtained. These results are consistent with the presence of a Na-Cl-K cotransport system in the medullary thick ascending limb of Henle's loop which may operate with a stoichiometry of 1/2/1.

Animals↗
PubMed1988

Dual effect of N-ethylmaleimide on Cl- transport across the thin ascending limb of Henle's loop.

Effects of SH reagents on Cl- transport were studied in the isolated hamster thin ascending limb of Henle's loop (TAL) perfused in vitro. Parachloromercuribenzene sulfonate (PCMBS) at 10(-4) M in the bath decreased the relative permeability for Cl-/Na+ (PCl/PNa), as determined by the transmural diffusion voltage (VT) generated under a NaCl concentration gradient, from 2.71 +/- 0.16 to 1.11 +/- 0.09 (P less than 0.001). The effect of PCMBS was prevented by the pretreatment with 10(-3) M dithiothreitol (DTT). N-Ethylmaleimide (NEM) at 10(-3) M in the bath exhibited a dual action on Cl- permeability of the TAL: It inhibited the Cl- permeability in fresh preparations, whereas it stimulated the Cl- permeability in the preparations pretreated with SH reagents including NEM, maleimide and PCMBS. The inhibitory effect was irreversible but the stimulatory effect was reversible. Both responses were prevented by DTT. Since dextran-maleimide did not show any inhibitory effect on PCl/PNa, the SH site responsible for the inhibition may be located inside of the cell. The stimulatory effect of NEM on PCl/PNa was markedly reduced when bath pH was reduced to 5.8. On the other hand, when the bathing fluid was made nominally Ca2+ free, the stimulatory effect of NEM was unaffected, although the basal level of PCl/PNa was reduced These observations suggest that the conductive Cl- pathway in the TAL is either stimulated or inhibited by modifying two distinct SH sites. The site of modulation by proton binding may exist distally to these SH sites. The regulatory mechanism involving Ca2+ may be independent of the SH regulatory sites.

4-Chloromercuribenzenesulfonate↗
PubMed1981

Sodium-chloride transport in the thick ascending limb of Henle's loop. Oxygen consumption studies in isolated cells.

Isolated cells were prepared from the medullary thick ascending limb of Henle's loop (TALH) and the response of oxygen consumption was correlated with the active chloride transport system found in these cells. Oxygen consumption was 31.6 microliters O2/mg protein . h and inhibited 50% by the absence of either sodium or chloride in the incubation medium. The absence of both sodium and chloride produced no further inhibition of oxygen consumption. Ouabain (10(-4) M) inhibited oxygen consumption by 50% and the inhibitory effect depended on the presence of both sodium and chloride in the incubation medium. Further, furosemide inhibited oxygen consumption by a maximum of 50% at 10(-3) M and also had no inhibitory effect if either sodium or chloride were absent. Furosemide had no effect on the Na, K-ATPase activity or ATP levels of the TALH cells. Thus, the data suggest or ATP levels of the TALH cells. Thus, the data suggest that 50% of the oxygen consumption of the TALH cells is related to the movement of sodium and chloride into the cell and that the ions may be transported in a coupled manner. In addition the effect of various diuretics on oxygen consumption in the isolated TALH cells was tested. The diuretics could be grouped in three categories: (1) highly effective in inhibiting chloride-dependent oxygen consumption with an apparent inhibitory constant (Ki) of around 10(-6) M, including the diuretics furosemide, bumetanide, ethacrynic acid-cysteine and piretanide, (2) diuretics which were less effective in inhibiting oxygen consumption with an apparent Ki of around 10(-4) M, HOE 740 and ethacrynic acid, and (3) diuretics which were ineffective in inhibiting chloride-dependent oxygen consumption, amiloride and hydrochlorothiazide.

Adenosine Triphosphate↗
PubMed1983

Flow-dependent water permeability of the rabbit descending limb of Henle's loop.

Because completely opposite results have been reported on the water permeability of the rabbit descending limbs of Henle's loop (DLH), we rigorously examined water permeability of the upper portion of the descending limb of the rabbit long-looped nephron. Even when the double-cannulation method was used in an attempt to reduce the resistance of tubular outflow, the collected fluid-to-perfusate inulin ratio was equal to or very close to the bathing fluid-to-perfusate osmolality ratio, indicating that osmotic equilibration occurred along the tubule by absorption of water. When perfusion rates were controlled by varying the height of the fluid reservoir connected to the perfusion pipette, osmotic (Pf) as well as diffusional (Pdw) water permeability was shown to be correlated with perfusion rate and/or perfusion pressure. Pf and Pdw at zero perfusion rate as determined from the values of the intercept of regression lines were 253 X 10(-3) and 4.54 X 10(-3) cm X s-1, respectively. The maximal values for Pf and Pdw were 737-1,098 X 10(-3) and 18.3 X 10(-3) cm X s-1, respectively. By changing the resistance to perfusion at the tubular outflow, it was shown that changes in Pf paralleled changes in perfusion rate rather than changes in perfusion pressure. Under stop-flow conditions the luminal fluid volume rapidly decreased after the osmolality of the bathing fluid was increased, suggesting that the segment is highly permeable to water even at zero flow rate. Reflection coefficients for urea and NaCl were 1.01 and 0.82, respectively. These data support the view that this segment is highly permeable to water and that increases in osmolality along the DLH in vivo may be accounted for mainly by abstraction of water rather than addition of solutes.

Animals↗
PubMed1998

Calcium-sensing receptor: regulation of electrolyte transport in the thick ascending limb of Henle's loop.

A calcium-sensing receptor (CaR) has functionally been described in the cortical thick ascending limb of Henle's loop (CTAL) of rat and mouse. This G protein-coupled receptor activates phospholipase C and increases the intracellular Ca2+ concentration. We observed that in the mouse CTAL cAMP formation, induced by 10(-8) mol/l AVP, was inhibited by more than 90% when the extracellular Ca2+ concentration ([Ca2+]e) was increased from 0.5 to 3 mmol/l. Measurements of transepithelial potential difference (PDte) in rat and mouse CTAL and medullary thick ascending limb (mTAL) segments and of transepithelial ion net fluxes in the mouse CTAL (isotonic perfusion conditions: 150 mmol/l NaCl in the lumen and bath) showed that an increase in the [Ca2+]e had no effect on basal and arginine vasopressin (AVP, 10(-10) mol/l)-stimulated transepithelial PDte, NaCl and Mg2+ transport. However, Ca2+ reabsorption was strongly inhibited by increased [Ca2+]e. Addition of AVP reversed this inhibitory effect of increased [Ca2+]e. Under hypotonic perfusion conditions (lumen 50 mmol/l NaCl; bath 150 mmol/l NaCl), a high [Ca2+]e induced a 50% decrease in Mg2+ reabsorption which was restored by AVP. Under these conditions, the effects on Ca2+ transport described above were still observed. In conclusion, activation of the CaR in the mouse TAL has no effect on basal and AVP-stimulated transepithelial NaCl reabsorption despite its large inhibitory effect on cAMP synthesis. The CaR, however, could play a role in the regulation of transepithelial Ca2+ and Mg2+ reabsorption.

Absorption↗
PubMed1988

Bartter's syndrome with a salt reabsorption defect in the cortical part of Henle's loop.

The pathogenesis of Bartter's syndrome remains uncertain. The prevailing theory postulates a defect in salt reabsorption, more frequently described in the thick ascending limb of Henle's loop. The patient we studied presents a normal urinary concentration capacity associated with impaired dilution, a free water clearance at the lower end of normal (5.4 ml/min/100 ml glomerular filtrate), a decreased distal fractional chloride reabsorption (54%) when studied during hypotonic saline diuresis, and a normal decrease in free water clearance after furosemide (2.1 ml/min/100 ml glomerular filtrate), suggesting a defect in the cortical part of Henle's loop. When studied during oral water diuresis, the fractional chloride reabsorption was normal (82%). This could be explained by a relative inability of the cortical diluting segment to reach maximal absorptive rates for NaCl. An inappropriate kaliuria related to an excessive delivery of salt load to the distal tubule is suggested by the correlation between urinary potassium and chloride excretion (r = 0.84; p less than 0.001). Aldosterone secretion participates also partially in the urinary potassium loss.

Absorption↗
PubMed1995

Cytosolic Ca2+ dynamics in hamster ascending thin limb of Henle's loop.

Intracellular calcium plays an important role in the regulation of Cl- reabsorption in the ascending thin limb of Henle's loop (ATL). To elucidate the cytosolic Ca2+ dynamics in the ATL, intracellular Ca2+ concentration activity ([Ca2+]i) was measured in the in vitro microperfused hamster ATL using fura 2. Basal [Ca2+]i was 89.1 +/- 7.3 nM (n = 9 tubules). Removal of Ca2+ from the peritubular solution decreased [Ca2+]i from 89.1 +/- 7.3 to 64.1 +/- 7.1 nM in 2 min (n = 9, P < 0.05), whereas [Ca2+]i did not change after removal of Ca2+ from the luminal solution. Addition of 1 mM NaCN to the bath increased [Ca2+]i. This effect was completely abolished by the elimination of ambient Ca2+. Trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) in the bath reversibly increased [Ca2+]i, whereas addition of 1 mM ouabain to the bath decreased [Ca2+]i. Rates of changes in [Ca2+]i after removal and replacement of basolateral Ca2+ were not affected by removal of Na+, K+, or Cl- from the bath, whereas nicardipine decreased these parameters. Increasing bath K+ from 5 to 100 mM decreased [Ca2+]i from 69.3 +/- 5.8 to 50.8 +/- 5.0 nM in 1 min (n = 6, P < 0.05). Subsequent reduction of K+ from 100 to 5 mM increased [Ca2+]i to 174.0 +/- 30.8 nM in 1 min, followed by a gradual decrease in [Ca2+]i to a steady-state level of 74.2 +/- 8.0 nM in 2 min. Changes in basolateral K+ concentration did not affect [Ca2+]i in the absence of ambient Ca2+.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Indinavir crystallization around the loop of Henle: experimental evidence.

OBJECTIVE: To determine the probable site of the nephron and the plasma indinavir (IDV) concentration at which intrarenal IDV crystallization occurs. DESIGN: We performed in vitro crystallization experiments in IDV solutions simulating conditions found in the nephron. METHODS: To determine intrarenal IDV concentrations at which conditions in the nephron allow crystallization, several concentrations of IDV basic solutions (0-800 mM) were titrated from pH 4.0 to higher pH values until crystals formed within 1 minute. Based on the combination of pH and ionic strength at which crystals formed, we determined the site of the nephron at which this combination was first attained. Based on the capacity for concentration at that site, we were able to measure the corresponding plasma IDV concentration. RESULTS: Under conditions normally found at the proximal tubule (i.e., pH 6.7 and ionic strength of 200 mM), IDV crystallized at 200 mg/L. Under conditions applying to the loop of Henle, pH 7.4 and ionic strength of 200 mM, IDV crystallized at 125 mg/L, which would correspond to a plasma IDV concentration of 8 mg/L. CONCLUSIONS: IDV crystallization is most likely in the loop of Henle and may already start at plasma IDV concentrations as low as 8 mg/L. Increasing hydration does not reduce the risk of IDV crystallization in the loop of Henle but instead prevents IDV crystallization and aggregation in the lower urinary tract. It remains to be confirmed whether prevention of high IDV plasma concentrations will reduce the risk of IDV crystallization in the loop of Henle.

Crystallization↗
PubMed1977

Effect of bumetanide and furosemide on the thick ascending limb of Henle's loop of rabbits and rats perfused in vitro.

Direct effects of bumetanide and furosemide on the thick ascending limb of Henle's loop (TALH) were compared by using the isolated tubules of rabbits and rats perfused in vitro. Both drugs, applied to the lumen, reversibly suppressed the lumen positive potential (PDt) of the rabbit TALH. Bumetanide also suppressed the PDt in the absence of Na+ where the NaCl of the artificial solutions was replaced by choline chloride. The efflux of 36Cl was also reduced by the addition of bumetanide to the perfusate. The dose-response analysis disclosed that bumetanide was 14 times as potent as furosemide. The onset and duration of bumetanide action was significantly longer than that of furosemide. Bumetanide also suppressed the PDt of the rat TALH when it was added to the perfusate.

Animals↗
PubMed1985

The vasopressin-sensitive adenylate cyclase in collecting tubules and in thick ascending limb of Henle's loop of human and canine kidney.

The major tubular effects of [8-Arg]vasopressin (AVP) in regulation of renal water excretion are initiated by stimulation of adenylate cyclase (AdC) coupled with V2 receptors. We explored whether the AVP-sensitive AdC is present in both collecting tubules and the thick ascending limb of Henle's loop of human and canine kidney. In cortical collecting tubule (CCT) and medullary collecting tubules (MCT) of human kidney, AdC was markedly stimulated by AVP [maximum change from basal level (delta), +2700%] and the the nonhormonal stimulatory agent forskolin (delta, +2000%). In human CCT, the effects of both compounds were synergistic. In contrast, AVP had no effect on AdC in either the medullary (MAL) or cortical (CAL) segment of the thick ascending limb of Henle's loop of human kidney; AVP also did not stimulate AdC in CAL or MAL in the presence of forskolin. Similar to that in the human kidney, in the canine kidney, AdC in CCT and MCT was markedly stimulated by AVP and forskolin (delta, +1000%), but AVP had no effect on AdC in CAL and MAL of the canine kidney. In intact tubules dissected from dog kidney and incubated in vitro, AVP markedly increased cAMP accumulation in MCT. AVP also elicited a small but detectable increase in cAMP accumulation in MAL. From these observations, we conclude that AVP-sensitive AdC is well developed in collecting tubules, but that AVP-sensitive AdC is absent in MAL and CAL of human kidney. Likewise, in canine nephron, the AVP-sensitive AdC of MAL and CAL is rudimentary or very labile. These findings suggest that the unresponsiveness of the AdC-cAMP system to AVP in segments of the thick ascending limb of Henle's loop may be a factor that accounts for a relatively low maximum osmotic concentration of urine which can be achieved by human or canine kidneys.

Adenylyl Cyclases↗
PubMed1988

Variant of Bartter's syndrome with a distal tubular rather than loop of Henle defect.

A 19-year-old normotensive patient had all of the clinical features of Bartter's syndrome: hypokalemia, elevated renin and aldosterone levels and increased excretion of prostaglandin E. In contrast to the patients described by Bartter, the patient had a normal capacity to form solute-free water, suggesting intact loop of Henle function. Baseline potassium and chloride excretion rates were higher than those observed in 5 normal subjects, but the response to intravenous chlorothiazide, a drug which acts in the early distal convolute tubule, was abnormal. While chloride excretion rose by only 61% in this patient, it increased sixfold in the normal subjects. Sodium excretion quadrupled in the controls but less than doubled in this patients. Roughly equivalent increments in potassium excretion occurred in normals and controls, suggesting that the patient's distal potassium-secretory mechanism was intact. Review of the literature indicates that whether the site of the abnormal renal tubular potassium (chloride) leak is the proximal tubule, the loop of Henle or the distal convoluted tubule, patients may achieve features indistinguishable from those previously reported as characteristic for Bartter's syndrome. If loop of Henle malfunction is required to diagnose classical Bartter's syndrome, then our patient (and several reported elsewhere) has a variant form.

Adult↗
PubMed1990

Tamm-Horsfall protein-mRNA synthesis is localized to the thick ascending limb of Henle's loop in rat kidney.

Tamm-Horsfall protein (THP) has been previously detected in cells of the thick ascending limb of Henle's loop (TAL) of different mammalian species using immunocytochemical methods. A nearly complete identity between THP and uromodulin, an immunosuppressive glycoprotein present in the urine of pregnant females, has been established recently. This paper describes the cellular location of THP mRNA by high-resolution in situ hybridization using a [35S]-labeled human uromodulin cRNA (antisense-) probe of a length of 665 base pairs. Control experiments were performed using an mRNA (sense-) probe of the same length. The probe was hybridized to frozen sections of the rat kidney. THP mRNA distribution in the kidney was found to be homologous to the immunocytochemical labeling pattern: Autoradiographic signal was present along the entire length of the TAL including the post-macula segment which leads to the distal convoluted tubule. Tubular cells of the macula densa were negative. Labeling intensity of the TAL epithelium was found to increase from the origin of the TAL at the transition between inner and outer medulla to its end beyond the macula densa. Labeling of the medullary segment in the inner stripe was weak, whereas outer medullary and cortical segments very strongly expressed THP mRNA. The glomerulus, the portions of the nephron proximal to the TAL, the distal convoluted tubule as well as the collecting duct system were negative.

Animals↗
PubMed1981

Presence of luminal K+, a prerequisite for active NaCl transport in the cortical thick ascending limb of Henle's loop of rabbit kidney.

Previous data from our laboratory have shown that active transport in the cortical thick ascending limb of Henle's loop (cTAL), as measured by the short circuit current (Lsc, microA X cm-2), requires the presence of Na+ and Cl-. The data were compatible with the model of secondarily active Cl- reabsorption involving the cotransport of Na+ and Cl- across the luminal membrane. The data suggested, furthermore, that 1 Na+ and 2 Cl- interact with the luminal carrier. In the present study it was tested whether this reabsorptive mechanism also requires the presence of luminal K+. Isolated cTAL segments (n = 40) were perfused at high flow rates with a modified Ringer's solution. Removal of K+ from the lumen reduced Isc significantly from 215 to 133 microA X cm-2. Addition of Ba2+ (10(-3) mol X 1(-1)) which blocks the K+ conductance of the luminal, membrane, to the K+-containing lumen perfusate decreased Isc significantly from 234 to 141 microA X cm-2. Combination of both manoeuvres: perfusion with a K+-free and Ba2+-containing solution almost abolished Isc from a control of 237 to 56 microA X cm-2. The results are compatible with the view that in rabbit cTAL the luminal carrier interacts with all 3 ions, possibly 1 Na+, 2 Cl-, and 1 K+. K+ recycles across the luminal membrane through its conductive pathway.

Animals↗
PubMed1996

Energy requirement of sodium reabsorption in the thick ascending limb of Henle's loop in the dog kidney: effects of bumetanide and ouabain.

To examine whether sodium reabsorption in the thick ascending limb of Henle's loop (TALH) in the dog kidney has a passive component, the ratios between reductions in sodium reabsorption and oxygen consumption (delta Na/delta Qo2 ratio) were measured by inhibiting tubular transport with bumetanide (30 micrograms kg-1) and ouabain (120 ng kg-1 intrarenally). Clearance studies were performed in volume expanded dogs treated with acetazolamide (100 mg kg-1) or maleate (400 mg kg-1). In five acetazolamide-treated dogs, bumetanide gave a delta Na/delta Qo2 ratio of 29.9 +/- 2.5, whereas the combination of bumetanide and ouabain gave 19.0 +/- 0.6. When ouabain was given before bumetanide, ouabain gave a delta Na/delta Qo2 ratio of 19.2 +/- 1.1 and the combination gave 19.9 +/- 1.2. In the maleate-treated dogs, bumetanide gave a delta Na/Qo2 ratio 30.3 +/- 1.7, and the combination of bumetanide and ouabain gave 27.1 +/- 1.5. To localize the metabolic effect of bumetanide and ouabain, local heat production was measured at 18 places in four kidneys with copper-constantan thermocouples. Bumetanide reduced metabolic rate in the outer medulla by 51 +/- 4%, and in the cortex by 16 +/- 6%. Subsequent infusion of ouabain reduced metabolic rate in the outer medulla by only 9 +/- 3%, whereas cortical metabolism was reduced by 33 +/- 4%. The results show that bumetanide mainly acts in the outer medullar where TALH is located, whereas the additional effect of ouabain is mainly located in cortical segment of the nephron including the proximal tubules. Bumetanide inhibits the reabsorption of 30 mol sodium for each mole oxygen consumed, which show that for each 18 mol sodium that are transported through the cells in the TALH in dog kidneys. 12 mol (40%) are transported along the paracellular route without additional requirement of energy.

Acetazolamide↗
PubMed1995

Amiloride-sensitive Na+/H+ antiporter in basolateral membrane of hamster ascending thin limb of Henle's loop.

The mechanisms of intracellular pH (pHi) regulation were investigated in the in vitro microperfused hamster ascending thin limb (ATL) of Henle's loop with the fluorescent pH indicator, 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. pHi of ATL cells was 7.05 +/- 0.02 (n = 30) when microperfused with a CO2/HCO(3-)-buffered solution. In HEPES-buffered solution, pHi was 7.10 +/- 0.02 (n = 16), which was significantly higher than the value in CO2/HCO(3-)-buffered solution (P < 0.05, n = 16). In HEPES-buffered solution, elimination of Na+ and addition of 1 mM amiloride to basolateral solution decreased the pHi by 0.12 +/- 0.03 (n = 6) and 0.11 +/- 0.02 (n = 5) at 1 min, respectively. The same manipulations in the luminal solution had no effect on pHi. One millimolar of N-ethylmaleimide (NEM) added to either side of ATL caused no significant change in pHi. Elimination of K+ on either side of ATL did not alter pHi. After adding 20 mM NH4Cl to basolateral solution, pHi instantaneously increased from 7.17 +/- 0.01 to 7.51 +/- 0.03 (n = 3), and then returned to steady-state level of 7.21 +/- 0.05 (n = 15) in 3 min. Removal of NH4Cl from basolateral solution then caused a rapid fall in pHi to 6.31 +/- 0.05 (n = 15), followed by spontaneous recovery at a rate of 0.43 +/- 0.06 unit/min (n = 15).(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed2006

The tight junction proteins claudin-7 and -8 display a different subcellular localization at Henle's loops and collecting ducts of rabbit kidney.

BACKGROUND: The tight junction (TJ) regulates the passage of ions and molecules through the paracellular pathway. In multicellular organisms, epithelial sheets function as a barrier between a variety of environments and the internal media. Therefore, TJs are required to control the passage of diverse molecules in different epithelia. The mammalian nephron constitutes a particularly relevant model of this diversity, since the paracellular transport in this organ is significantly different along the various tubular segments. Here, we have analysed the distribution of claudins-7 and -8 in Henle's loops and collecting ducts isolated from rabbit kidneys. METHODS: Renal segments were manually isolated from newborn and adult rabbit kidneys and processed for immunofluorescence. The distribution of claudins-7 and -8 was studied by confocal microscopy. RESULTS: The localization of claudins-7 and -8 along Henle's loops and collecting ducts is remarkably different. While claudin-8 displays a clear cell border distribution in Henle's segment, claudin-7 shows a non-specific cytosolic staining. Moreover, in the collecting ducts, claudin-8 localizes at the TJ region, while claudin-7 shows a basolateral staining. This pattern is present from the newborn stage. The distribution of claudins along the mammalian kidney has been found to vary in different mammalian species. Accordingly, in the rabbit, we have found the expression of claudin-8 at the descending and ascending thin limbs of Henle, a distribution that differs from that found in the mouse by others. CONCLUSION: In the rabbit Henle's loop, claudin-8 is present at the cellular borders of the descending and ascending thin limbs, while claudin-7 displays no specific labelling. Instead, at the collecting duct, both claudins are present but exhibit a different subcellular distribution.

Animals↗