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PubMed1988

Effect of Ca2+ on Cl- transport in thin ascending limb of Henle's loop.

Effects of ambient Ca2+ concentration on Cl- transport across the thin ascending limb of Henle's loop (TAL) were examined by the in vitro microperfusion technique. When Ca2+ concentration in the bathing fluid was decreased from 1.5 mM to nominally 0 mM at 37 degrees C, the relative permeability of Cl- to Na+ (PCl/PNa) estimated from the NaCl diffusion voltage changed from 2.44 +/- 0.20 to 1.27 +/- 0.16 (n = 7, P less than 0.01). When Ca2+ concentration of the luminal fluid was reduced, PCl/PNa was unchanged. When Ca2+ concentration in the bathing fluid was changed from 4.5 to nominally 0 mM, the lumen-to-bath flux coefficient for 36Cl (K36Cl(l----b)) was decreased, whereas the value for 22Na was unchanged, indicating that the reduction of Ca2+ concentration in the bathing fluid selectively inhibits Cl- transport without affecting Na+ transport. By contrast, at 23 degrees C, the elimination of Ca2+ from the bathing fluid caused only a small reduction of PCl/PNa. Although at 23 degrees C acidification of the bathing fluid caused only little or no decrease in Cl- permeability, the elimination of Ca2+ from the bathing fluid under acid pH markedly suppressed the (K36Cl(l----b)) (10(-7) cm2/s). The pH titration curves of relative Cl- permeability examined at three different Ca2+ concentrations at 37 degrees C revealed that the interaction between proton and Ca2+ was noncompetitive. Addition of quin 2-AM, which reduced intracellular Ca2+ concentration, to the bath caused an irreversible suppression of Cl- permeability, suggesting that the decrease in intracellular Ca2+ concentration also inhibits the Cl- transport across the TAL.(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗

PubMed1990

Effect of azosemide on the in vitro perfused thick ascending limb of Henle's loop from the mouse.

Direct effect of azosemide on the mouse thick ascending limb of Henle's loop was examined by the isolated tubules perfusion technique, and the effect was compared with that of furosemide. Azosemide added to the tubular lumen reversibly suppressed the lumen positive potential (PDt) and decreased the net chloride reabsorption. Dose-response studies of these two drugs suggested that azosemide was about 5 times as potent as furosemide. The more potent effect of azosemide compared with furosemide was confirmed by a paired study in the same tubules. At a concentration of 10(-5) mol/l azosemide suppressed PDt by 91.4%, furosemide by 65.6%.

Animals↗

PubMed1984

Effects of enantiomers of indacrinone (MK-196) on cation transport by the loop of Henle and distal tubule studied by microperfusion in vivo.

We have studied the effects of the two enantiomeric forms of the diuretic agent, indacrinone (MK-196), upon transport of sodium and potassium by the loop of Henle and distal tubule, using the technique of continuous microperfusion, in vivo, of individual tubular segments in the rat kidney. In the loop of Henle, both the (+)-and (-)-enantiomers, when included in the tubular perfusion fluid at a concentration of 5 X 10(-4) M, inhibited the reabsorption of sodium and potassium, but the (-)-enantiomer was significantly more effective in this regard than the (+)-enantiomer. Although loop sodium reabsorption was incompletely blocked by either form of the drug, potassium reabsorption by the loop was on average abolished by (-)-MK-196 and was actually converted in some experiments to an appreciable net secretory flux. In the distal tubule, both enantiomers inhibited net sodium reabsorption, but neither affected the control level of potassium secretion. These experiments provide direct evidence that the natriuretic effect of this agent is due to actions on sodium transporting sites in the loop of Henle and distal tubule. Furthermore, because potassium transport was affected only in the loop, they suggest that the nature of the cellular cation transport mechanism influenced by the drug may be different at the two nephron sites studied.

Animals↗

PubMed1995

Bicarbonate transport along the loop of Henle effects of adrenal steroids.

The role of adrenal steroids in the regulation of bicarbonate absorption in the loop of Henle was studied by in vivo microperfusion. Bicarbonate transport (JHCO3) was measured by microcalorimetry and fluid reabsorption by [14C]inulin, 7-10 days after surgery, in 1) sham-operated control rats, 2) adrenalectomized (Adx) rats, 3) Adx rats receiving dexamethasone (1.2 micrograms.100 g body wt-1.24 h-1) and a low dose of aldosterone (0.5 micrograms.100 g body wt-1.24 h-1), 4) Adx rats receiving dexamethasone, 5) Adx rats receiving a low dose of aldosterone, and 6) Adx rats receiving a high dose of aldosterone (1.0 micrograms.100 g body wt-1.24 h-1). JHCO3 along the loop of Henle was decreased by 40% in Adx rats. JHCO3 was increased by dexamethasone alone and by dexamethasone plus a low dose of aldosterone to rates observed in fully supplemented Adx rats. Aldosterone given alone at a low physiological dose had no effect, but, when administered at a high dose, returned JHCO3 to normal.

Absorption↗

PubMed1998

Contribution of Na+-H+ exchange to sodium reabsorption in the loop of henle: a microperfusion study in rats.

1. The contribution of apical Na+-H+ exchange to sodium reabsorption in the thick ascending limb of the loop of Henle (TALH) in vivo was examined in anaesthetized rats by perfusing loops of Henle of superficial nephrons with solutions containing the Na+-H+ exchange inhibitor, ethyl isopropyl amiloride (EIPA). 2. Using a standard perfusate, no statistically significant effect of EIPA on net sodium reabsorption (JNa) was detected. However, when sodium reabsorption in the pars recta of the proximal tubule was minimized by using a low-sodium perfusate, EIPA reduced JNa from 828 +/- 41 to 726 +/- 37 pmol min-1 (P < 0.05), indicating that apical Na+-H+ exchange can make a small contribution to net sodium reabsorption in the TALH in vivo. This contribution appears to be dependent on the bicarbonate load, since an increase in the latter led to an enhancement of EIPA-sensitive sodium transport. 3. Addition of the Na+-K+-2Cl- cotransport inhibitor, bumetanide, to the low-sodium perfusate reduced baseline JNa to 86 +/- 27 pmol min-1. In this setting, EIPA reduced JNa further, to -24 +/- 18 pmol min-1 (P < 0.05), an effect similar to that seen in the absence of bumetanide. This finding argues against previous suggestions (based on in vitro evidence) that inhibition of the Na+-K+-2Cl- cotransporter leads to an increase in apical Na+-H+ exchange in the TALH.

Amiloride↗

PubMed1991

Sodium and potassium load in the loop of Henle, measured with intact and blocked tubuloglomerular feedback mechanism in juxtamedullary nephrons.

For the juxtamedullary nephrons only the loop of Henle is easily accessible for micropuncture. We have shown that the tubuloglomerular feedback (TGF) mechanism is highly activated in these nephrons. Techniques have been developed for measurements on these nephrons without disrupting the normal flow to the macula densa. The tubular flow rate was measured by a real-time videodensitometric method in juxtamedullary nephrons in Lewis x DA rats. For the determination of tubular fluid composition a small fraction (less than 10%) of the fluid was sampled. Measurements were also performed according to the conventional technique, where all the tubular fluid was sampled. Despite a more than twofold increase in tubular flow rate when the flow to the macula densa region was interrupted, sodium concentration was only reduced by 25%, whereas potassium concentration was reduced by 40%. The results demonstrate that interruption of the urine flow to the macula densa results in a 52% increase in the tubular load of Na in the loop of Henle of juxtamedullary nephrons, and a corresponding increase of 24% for K. Thus, TGF exerts a strong influence on these nephrons which is why previous data on water and electrolyte loads, based on stop-flow measurements, greatly overestimate these loads.

Animals↗

PubMed1995

Effect of NH4+/NH3 on cytosolic pH and the K+ channels of freshly isolated cells from the thick ascending limb of Henle's loop.

The conductance properties of the luminal membrane of cells from the thick ascending limb of Henle's loop of rat kidney (TAL) are dominated by K+. In excised membrane patches the luminal K+ channel is regulated by pH changes on the cytosolic side. To examine this pH regulation in intact cells of freshly isolated TAL segments we measured the membrane voltage (Vm) in slow-whole-cell (SWC) recordings and the open probability (Po) of K+ channels in the cell-attached nystatin (CAN) configuration, where channel activity and part of Vm can be recorded. The pipette solution contained K+ 125 mmol/l and Cl- 32 mmol/l. Intracellular pH was determined by 2',7'bis(2-carboxyethyl)-5,(6)-carboxyfluorescein (BCECF) fluorescence. pH changes were induced by the addition of 10 mmol/l NH4+/NH3 to the bath. In the presence of NH4+/NH3 intracellular pH acidified by 0.53 +/- 0.11 units (n = 7). Inhibition of the Na+2Cl-K+ cotransporter by furosemide (0.1 mmol/l) reversed this effect and led to a transient alkalinisation by 0.62 +/- 0.14 units (n = 7). In SWC experiments Vm of TAL cells was -72 +/- 1 mV (n = 70). NH4+/NH3 depolarised Vm by 22 +/- 2 mV (n = 25). In 11 SWC experiments furosemide (0.1 mmol/l) attenuated the depolarising effect of NH4+ from 24 +/- 3 mV to 7 +/- 3 mV. Under control conditions the single-channel conductance of TAL K+ channels in CAN experiments was 66 +/- 5 pS and the reversal voltage for K+ currents was 70 +/- 2 mV (n = 35). The Po of K+ channels in CAN patches was reduced by NH4+/NH3 from 0.45 +/- 0.15 to 0.09 +/- 0.07 (n = 7). NH4+/NH3 exposure depolarised the zero current voltage of the permeabilised patches by -9.7 +/- 3.6 mV (n = 5). The results show that TAL K+ channels are regulated by cytosolic pH in the intact cell. The cytosolic pH is acidified by NH4+/NH3 exposure at concentrations which are physiologically relevant because Na+2Cl-K+(NH4+) cotransporter-mediated import of NH4+ exceeds the rate of NH3 diffusion into the TAL. K+ channels are inhibited by this acidification and the cells depolarise. In the presence of furosemide TAL cells alkalinise proving that NH4+ uptake occurs by the Na+2Cl-K+ cotransporter. The findings that, in the presence of NH4+/NH3 and furosemide, Vm is not completely repolarised and that K+ channels are not activated suggest that the respective K+ channels may in addition to their pH regulation be inhibited directly by NH4+/NH3.

Ammonia↗

PubMed1984

Functional heterogeneity of the descending limbs of Henle's loop. II. Interspecies differences among rabbits, rats, and hamsters.

Permeability properties of the descending limbs of Henle's loop were compared among rabbits, hamsters, and rats by measuring transepithelial voltage (Vt) across the isolated renal tubules perfused in vitro. From the deflection of the Vt when the composition of the bathing fluid was varied, the permeabilities of sodium and of potassium relative to chloride (Pna/PCl and PK/PCl, respectively) were determined in either the descending limbs of the short-loop nephron (SDL) or the segments of the upper protion of the long-loop nephron (LDLu). In hamsters and rats, the values of PNa/PCl of the LDLu (3.98 +/- 0.66 and 5.03 +/- 0.79) were higher than those of the SDL (0.68 +/- 0.03 and 0.61 +/- 0.00). In contrast, in rabbits the value of PNa/PCl of the LDLu (0.96 +/- 0.05) was only slightly higher than that of the SDLu (0.75 +/- 0.03). The similar tendency was also noted in the values of PK/PCl. In hamsters and rats, the PK/PCi ratios were 4.90 +/- 0.82 and 6.44 +/- 0.90, respectively, in the LDLu and 1.09 +/- 0.04 and 1.02 +/- 0.0, respectively in the SDL. When a transepithelial osmotic gradient was imposed by adding raffinose to the bath, a lumen-negative streaming voltage of about -8 mV was generated in the hamster and the rat LDLu. Taken together with the findings in the preceding paper, these observations support the view that the descending limbs of rabbits are different from those of hamsters and rats in that internephron heterogeneity is less remarkable, and that the LDLu of hamsters and rats is highly permeable to sodium and to potassium as well as to water.

Animals↗

PubMed2000

Intracellular pH in isolated rat renal papillary thin limbs of Henle's loop.

Intracellular pH (pHi) was measured in isolated, nonperfused and perfused rat papillary thin limbs of Henle's loops in N-2-hydroxyethylpiperazine-N'-2-ethansulfonic acid (HEPES)- or HEPES/bicarbonate-buffered medium at pH 7.4 using the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF). Resting pHi was about 6.7 in descending thin limbs (DTL) and about 6.9 in ascending thin limbs (ATL), even with a medium pH of 7.4. These values appeared to reflect the acid pH of the blood in the neighboring vasa recta found in vivo. The resting pHi did not differ whether or not the medium contained bicarbonate although the total buffering capacity of the tubule cells was increased in the presence of bicarbonate. In nonperfused DTL and ATL, pHi was further acidified following an NH4Cl pulse. The rate of recovery of pHi from this level to the resting pHi was reduced by Na+ removal from the bath in both DTL and ATL and by the addition of ethylisopropylamiloride (EIPA) to the bath in the presence of Na+ in DTL. The rate of recovery was not affected by Cl- removal from the bath or K+ (75 mM) or 4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS) addition to the bath in either DTL or ATL. These results suggest that the common, amiloride-sensitive, basolateral Na+/H+ exchanger plays a role in the regulation of pHi in rat papillary DTL but that a different basolateral Na+/H+ exchanger or a luminal Na+/H+ exchanger is important in rat papillary ATL.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1989

Cells in culture from rabbit medullary thick ascending limb of Henle's loop.

Freshly isolated cells obtained from the medullary segment of the rabbit thick ascending limb of Henle's loop (mTALH) metabolize arachidonic acid (AA) primarily by the cytochrome P-450 monooxygenase pathway forming several products; a vasorelaxant and an inhibitor of Na+-K+-ATPase have been identified. These studies have been extended to mTALH cells in culture. The ability of cells isolated from 1-mo-old rabbits to grow in culture far surpassed that of cells isolated from adult rabbits, whereas similar cytochrome P-450-dependent AA metabolites were produced by freshly isolated cells from rabbits of both ages. Three-week-old mTALH cultures formed ouabain-sensitive "domes" when grown on plastic surfaces and developed transepithelial voltages (4.7 + 1.2 mV, n = 6) when grown on gas-permeable surfaces. Electron microscopy of the cells showed typical mTALH cell characteristics. The presence of Tamm-Horsfall protein, a surface membrane protein of mTALH cells, in 90-95% of the cells confirmed the homogeneity of the cultures. Although several environmental manipulations were tested, mTALH cells in culture did not produce the same cytochrome P-450-dependent AA metabolites as those produced by mTALH cells before culture. However, a cytochrome P-450-dependent AA metabolite that differs from the AA metabolites formed by freshly isolated mTALH cells was produced by hemin-treated mTALH and heterogenous cell cultures.

Animals↗

PubMed1988

Evidence for conductive Cl- pathways across the cell membranes of the thin ascending limb of Henle's loop.

To examine whether Cl- is transported via transcellular pathways in the thin ascending limb of Henle's loop (TAL), conventional microelectrode technique was applied in isolated TAL segments of hamsters perfused in vitro. The average basolateral membrane voltage (VB) was -24.5 +/- 1.5 mV (n = 18). Ouabain (10(-4) M) had no effect on VB. Sudden reduction of basolateral Cl- concentration from 165 to 5 mmol/liter caused a large depolarizing spike (+49.1 +/- 2.7 mV, n = 18), while the transepithelial potential (VT) showed lumen positive deflection by 33.4 +/- 1.2 mV, which indicates that a large Cl- conductance exists in the basolateral membrane. Reduction of luminal Cl- concentration caused sustained depolarization of luminal cell membrane from +24.5 +/- 2.1 to -9.7 +/- 3.4 mV (n = 6), which indicates that there is also a Cl- conductance in the luminal membrane. Since we have previously shown that acidification of ambient solution suppresses the transmural Cl- permeability, we tested whether acid pH also inhibits the Cl- conductance of the basolateral membrane. When pH of the bathing fluid was lowered to 5.8, the depolarizing spike of VB and the change of VT upon sudden reduction of basolateral Cl- were almost completely abolished. From these results we conclude: (a) both the luminal and the basolateral membrane of hamster TAL segments have Cl- conductances, and (b) Cl- transport in the TAL takes place, at least in part, via a transcellular route when a transepithelial Cl- gradient is present.

Animals↗

PubMed1991

Effect of cytochrome P450 arachidonate metabolites on ion transport in rabbit kidney loop of Henle.

In the medullary segment of the thick ascending limb of the loop of Henle (mTALH), arachidonic acid (AA) is metabolized by a cytochrome P450-dependent monooxygenase to products that affect ion transport. The linkage between changes in ion transport and AA metabolism in isolated cells of the mTALH was examined. AA produced a concentration-dependent inhibition of 86Rb uptake--an effect that was prevented by selective blockade of cytochrome P450 monooxygenases. Inhibition by cytochrome P450 blockade of the effect of AA on 86Rb uptake could be circumvented by addition of the principal products of AA metabolism in the mTALH.

Animals↗

PubMed1991

Bicarbonate transport along the loop of Henle. I. Microperfusion studies of load and inhibitor sensitivity.

We microperfused the loop of Henle (LOH) to assess its contribution to urine acidification in vivo. Under control conditions (Na HCO3- = 13 mM, perfusion rate approximately 17 nl/min-1) net bicarbonate transport (JHCO3-) was unsaturated, flow- and concentration-dependent, and increased linearly until a bicarbonate load of 1,400 pmol.min-1 was reached. Methazolamide (2 x 10(-4) M) reduced JHCO3 by 70%; the amiloride analogue ethylisopropylamiloride (EIPA) (2 x 10(-4) M) reduced JHCO3 by 40%; neither methazolamide nor EIPA affected net water flux (Jv). The H(+)-ATPase inhibitor bafilomycin A1 (10(-5) M) reduced JHCO3 by 20%; the Cl- channel inhibitor 5-nitro-2'-(3-phenylpropylamino)-benzoate (2 x 10(-4) M) and the Cl(-)-base exchange inhibitor diisothiocyanato-2,2'-stilbenedisulfonate (5 x 10(-5) M), had no effect on fractional bicarbonate reabsorption. Bumetanide (10(-6) M) stimulated bicarbonate transport (net and fractional JHCO3-) by 20%, whereas furosemide (10(-4) M) had no effect on bicarbonate reabsorption; both diuretics reduced Jv. In summary: (a) the LOH contributes significantly to urine acidification. It normally reabsorbs an amount equivalent to 15% of filtered bicarbonate; (b) bicarbonate reabsorption is not saturated; (c) Na(+)-H+ exchange and an ATP-dependent proton pump are largely responsible for the bulk of LOH bicarbonate transport.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1994

The effect of acute metabolic alkalosis on bicarbonate transport along the loop of Henle. The role of active transport processes and passive paracellular backflux.

The loop of Henle (LOH) reabsorbs approximately 15% of filtered HCO3- via a luminal Na(+)-H+ exchanger and H+ATPase. During acute metabolic alkalosis (AMA) induced by i.v. HCO3- infusion, we have observed previously inhibition of LOH net HCO3- reabsorption (JHCO3-), which contributes to urinary elimination of the HCO3- load and correction of the systemic alkalosis. To determine whether the activities of the Na(+)-H+ exchanger and/or H(+)-ATPase are reduced during AMA, two inhibitors believed to be sufficiently specific for each transporter were delivered by in vivo LOH microperfusion during AMA. AMA reduced LOH JHCO3- from 205.0 +/- 10.8 to 96.2 +/- 11.8 pmol.min-1 (P < 0.001). Luminal perfusion with bafilomycin A1 (10(-4) mol.l-1) caused a further reduction in JHCO3- by 83% and ethylisopropylamiloride (EIPA; 5.10(-4) mol.l-1) completely abolished net HCO3- reabsorption. The combination of bafilomycin A1 and EIPA in the luminal perfusate was additive, resulting in net HCO3- secretion (-66.6 +/- 20.8 pmol.min-1; P < 0.001) and abolished net fluid reabsorption (from 5.0 +/- 0.6 during AMA to 0.2 +/- 1.1 nl.min-1; P < 0.001). To establish whether HCO3- secretion via luminal stilbene-sensitive transport mechanism participates in LOH adaptation to AMA, we added diisothiocyanato-2,2'-stilbenedisulphonate (DIDS; 10(-4) mol.l-1) to the perfusate. No effect was found.(ABSTRACT TRUNCATED AT 250 WORDS)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1987

Magnesium reabsorption in the juxtamedullary loop of Henle: effect of magnesium deprivation.

To determine the contribution of the juxtamedullary loop of Henle to magnesium reabsorption during magnesium deficiency, we performed two-phase micropuncture studies of end-descending limbs in a group of magnesium-deficient rats (n = 7) and in a pair-fed control group (n = 8) given MgCl2 in their drinking water. In the magnesium-deficient rats, daily excretion of magnesium fell to very low values (1.2 +/- 0.2 vs. 52 +/- 12 microM.day-1.100 g body weight-1, p less than 0.05). Plasma magnesium concentration and fractional magnesium excretion during the control phase were nearly 52 and 27%, respectively, of the values observed in pair-fed controls. Fractional magnesium delivery to the end-descending limb did not differ significantly between the two groups. During the acute magnesium repletion phase, fractional magnesium excretion and fractional magnesium delivery to the end-descending limb increased by a similar value in the two groups of rats, despite a lower filtered load of magnesium in the magnesium-deficient group. Absolute magnesium reabsorption upstream to the end-descending limb was lower in the magnesium-deficient rats but was otherwise tightly coupled to the filtered load of magnesium (Y = 0.91 + 0.37 x, r = 0.82, p less than 0.05). Similar observations were made with regards to whole kidney magnesium reabsorption. Our results suggest that, in young magnesium-deficient rats, magnesium reabsorption is tightly coupled to the filtered load of magnesium both in segments upstream to the juxtamedullary end-descending limb and in the whole kidney, and that a reabsorptive defect for magnesium is not evident in this setting.

Animals↗

PubMed2001

Regulation of intracellular pH in rat renal inner medullary thin limbs of Henle's loop.

Regulation of intracellular pH (pHi) was studied in isolated rat renal inner medullary thin limbs of Henle's loop in bicarbonate/phosphate-buffered medium with high pCO2, high osmolality ( congruent with670 mosmol/kg H2O; 270 mM urea; 180 mM NaCl), organic osmolytes, and a pH of 6.8 to approximate the physiological in vivo environment. The pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF) was used to measure pHi. Resting pHi was always acid and significantly more acid in descending thin limb (DTL) cells than in ascending thin limb (ATL) cells from pure or mixed-type thin limbs. Resting pHi was slightly but significantly higher in both DTLs and ATLs in high osmolality ( approximately 670 mosmol/kg H2O) than in low osmolality ( approximately 290 mosmol/kg H2O) medium but not when sucrose replaced urea. In both DTLs and ATLs the rate of recovery of pHi following additional acidification with an NH4Cl pulse was reduced by Na+ removal from the medium and by the addition of 60 microM HOE642 (an inhibitor of the Na+/H+ exchanger, NHE1), 55 microM S1611 (inhibitor of Na+/H+ exchanger, NHE3), 1 microM bafilomycin A1 (an inhibitor of vacuolar H+ -ATPase), or 20 microM Schering 28080 (an inhibitor of H+ -K+ -ATPase) to the medium. Resting pHi was also reduced by 60 microM HOE642, 55 microM S1611, and 20 microM Schering 28080. In both DTLs and ATLs, RT-PCR revealed message for NHE1, NHE3, and vacuolar H+ -ATPase; immunocytochemistry demonstrated the expression of the protein for NHE1 (basolateral membrane), NHE3 (luminal membrane), and H+ -K+ -ATPase (luminal membrane). These data suggest that pHi in rat inner medullary thin limbs is regulated by urea and by basolateral and luminal H+ extrusion via NHE1, NHE3, vacuolar H+ -ATPase, and H+ -K+ -ATPase.

Acid-Base Equilibrium↗

PubMed1987

Effect of pH on Cl- transport in TAL of Henle's loop.

To further characterize the mechanism of Cl- transport across the hamster thin ascending limb (TAL) of Henle's loop, we examined effects of pH on Cl- permeability as determined by either the choline chloride diffusion voltage or the lumen-to-bath 36Cl flux in the isolated segments perfused in vitro. When pH of the bathing fluid or the perfusate was reduced from 7.4 to 5.8, the Cl(-)-Na+ permeability ratio (PCl/PNa) was reduced from 2.77 +/- 0.21 to 0.48 +/- 0.02 (n = 7, P less than 0.01) or from 2.55 +/- 0.15 to 0.81 +/- 0.11 (n = 6, P less than 0.01), respectively. At 37 degrees C, when the pH of the bathing fluid was reduced from 7.4 to 6.2, the lumen-to-bath flux coefficient for 36Cl (X10(-7) cm2/s) was reduced from 84.8 +/- 7.5 to 20.4 +/- 3.2 (n = 7, P less than 0.01), whereas the value for 22Na was unchanged (27.3 +/- 2.9 vs. 25.3 +/- 2.5, n = 5). From the pH titration curves for PCl/PNa, pKa values for proton binding were 6.31 and 5.78, and Hill's coefficients were 2.1 and 2.3 on the basolateral side and on the luminal side, respectively. Alkalinization had little or no effect on the Cl- permeability. At room temperature, the acid pH did not affect the Cl- permeability. Intracellular acidification with o-nitrophenylacetate also decreased the Cl- permeability.(ABSTRACT TRUNCATED AT 250 WORDS)

Algorithms↗

PubMed1995

ANG II is a mitogen for a murine cell line isolated from medullary thick ascending limb of Henle's loop.

A murine SV40-transformed renal epithelial cell line derived from medullary thick ascending limb of Henle's loop (MTAL) was established and characterized by morphology, antigen expression, and biochemical criteria. These MTAL cells express a single class of high-affinity receptors for angiotensin II (ANG II) and transcripts for the AT1 subtype of ANG II receptors. ANG II, in a dose-dependent manner, induced proliferation of MTAL cells. This observation is in striking contrast to syngeneic proximal tubular cells in which it was previously shown that the peptide induced cellular hypertrophy and slightly inhibited proliferation [G. Wolf and E. G. Neilson. Am. J. Physiol. 259 (Renal Fluid Electrolyte Physiol. 28: F768-F777, 1990]. The AT1-receptor antagonist losartan (10(-6) M), but not an AT2-receptor antagonist, blocked the mitogenic effects of ANG II in MTAL cells. Coincubation of quiescent MTAL cells with ANG II and 5% fetal calf serum further increased proliferation compared with cells grown only in serum. In contrast to proximal tubular cells, ANG II failed to induce transforming growth factor-beta 1 mRNA and protein synthesis in MTAL cells. Our data collectively suggest that ANG II is a mitogen for MTAL cells in vitro. Therefore, epithelial cells derived from different parts of the nephron, even when transformed with SV40 virus and while under cell culture conditions, exhibit a distinct pattern of growth behavior after stimulation with ANG II.

Angiotensin II↗