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PubMed2004

Regulation of the Cl-/HCO3- exchanger AE2 in rat thick ascending limb of Henle's loop in response to changes in acid-base and sodium balance.

The Cl(-)/HCO(3)(-) exchanger AE2 is believed to be involved in transcellular bicarbonate reabsorption that occurs in the thick ascending limb of Henle's loop (TAL). The purpose of this study was to test whether chronic changes in acid-base status and sodium intake regulate AE2 polypeptide abundance in the TAL of the rat. Rats were subjected to 6 d of loading with NaCl, NH(4)Cl, NaHCO(3), KCl, or KHCO(3). AE2 protein abundance was estimated by semiquantitative immunoblotting in renal membrane fractions isolated from the cortex and the outer medulla of treated and control rats. In the renal cortex, AE2 abundance was markedly increased in response to oral loading with NH(4)Cl or with NaCl. In contrast, AE2 abundance was unchanged in response to loading with KCl or with NaHCO(3) and was decreased by loading with KHCO(3). The response of AE2 in the outer medulla differed from that in the cortex in that HCO(3)(-) loading increased AE2 abundance when administered with Na(+) but had no effect when administered with K(+). Immunohistochemistry revealed that NaCl loading increased AE2 abundance in the basolateral membrane of both the cortical and the medullary TAL. In contrast, NH(4)Cl loading increased AE2 abundance only in the cortical TAL but not in the medullary TAL. These results suggest that regulation of the basolateral Cl(-)/HCO(3)(-) exchanger AE2 plays an important role in the adaptation of bicarbonate absorption in the TAL during chronic acid-base disturbances and high sodium intake. The present study also emphasizes the contribution of cortical TAL adaptation in the renal regulation of acid-base status.

Acid-Base Equilibrium↗
PubMed1994

Polylactosamine sugar chains expressed by epithelia of Henle's loop and collecting duct in rat and human kidney are selectively recognized by human cold agglutinins anti-I/i.

Normal rat and human kidney was mapped immunohistochemically with human monoclonal cold agglutinins against the biochemically related erythrocyte glycoconjugate antigens I and i, which represent branched and linear polylactosamines, respectively. The antibodies worked well with both cryostat and paraffin-embedded material. Anti-i gave specific staining of collecting duct cells (mostly principal cells) as evidenced by double labelling with antibodies to band 3 and a 23 kD protein of intercalated cells. In contrast, anti-I turned out to be the first exclusive marker for the ascending and descending thin limb of Henle's loop. In addition, in rat kidney, the binding of anti-I/i was preserved in primary cultures both of principal cells of the papillary collecting duct and cells of the thin limb of Henle's loop. Our results suggest that both antibodies might be interesting tools for in vitro studies of renal cell physiology and the investigation of kidney development.

Agglutinins↗
PubMed1991

Vasopressin stimulation of NaCl transport in the medullary thick ascending limb of Henle's loop is decreased in aging mice.

The maximal urinary osmolality that can be reached by the kidney is reduced with age. This may be due to impaired NaCl transport by the medullary thick ascending limb of Henle's loop, which is part of the renal concentrating mechanism and is modulated by antidiuretic hormone (ADH). We therefore tested in vitro a possible age-related change in the transport capacity and in the response of this nephron segment to ADH in young (1-2 months) and old (20-24 months) mice. The transepithelial potential difference (Vte) was significantly higher in young mice (+8.5 +/- 0.4 mV, n = 13) than in old ones (+6.6 +/- 0.5 mV, n = 17). Addition of 0.1 nmol.1-1 ADH to the bath solution significantly increased Vte by 5.2 +/- 0.5 mV in the young and by 3.1 +/- 0.6 mV in the old animals. Application of dibutyryl-cAMP (0.1 mmol.1-1) did not further increase the hormonal response in both groups. The ADH-mediated increase in the corresponding equivalent short-circuit current (ISC = Vte/Rte) was twice as great in young mice as in old, indicating that the stimulation of NaCl transport by ADH across the medullary thick ascending limb is significantly reduced with age. These results suggest that the previously reported age-related defect in the urinary concentrating ability of the kidney is partly due to a decreased response of the medullary thick ascending limb to ADH.

Aging↗
PubMed1989

Regulation of cAMP metabolism by PGE2 in cortical and medullary thick ascending limb of Henle's loop.

We have examined the regulation by prostaglandin E2 (PGE2) of hormone-induced adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in cells isolated by immunodissection from both the medullary and cortical thick ascending limb of Henle's loop of rabbit kidney. At concentrations greater than 10(-8) M, PGE2, but not sulprostone (16-phenoxy-17,18,19,20-tetranor-PGE2 methylsulfonilamide), caused cAMP accumulation in both cortical and medullary thick limb cells. However, at concentrations of less than or equal to 10(-8) M, both PGE2 and sulprostone inhibited arginine vasopressin (AVP)-, calcitonin-, and glucagon-induced cAMP accumulation in medullary thick ascending limb (mTAL) cells. In cortical thick limb (cTAL) cells, sulprostone also inhibited AVP-, calcitonin-, and parathyroid hormone (PTH)-induced cAMP accumulation. The inhibitory effects of PGE2 and of sulprostone were blocked by pretreatment of mTAL and cTAL cells with pertussis toxin. Membranes prepared from mTAL cells exhibited a [3H]PGE2 binding activity that was stimulated on addition of the stable guanosine 5'-triphosphate (GTP) analogue, 5'-guanosine gamma-thiotriphosphate (GTP gamma S); moreover, sulprostone inhibited [3H]PGE2 binding. Our results suggest that PGE2 can function via a prostaglandin E receptor linked to a guanine nucleotide regulatory protein, Gi, to attenuate hormone-induced cAMP formation in both mTAL and cTAL cells of rabbit kidney.

Animals↗
PubMed1987

A Ca2-activated cation-selective channel in the basolateral membrane of the cortical thick ascending limb of Henle's loop of the mouse.

The patch-clamp technique was used to investigate the properties of a cation-selective channel in the basolateral membrane of microdissected collagenase-treated fragments of cortical thick ascending limbs of Henle's loop from mouse kidney. The channel activity was seldom observed in cell-attached patches (2 out 15 studied cases). In inside-out excised patches immersed in symmetrical NaCl Ringer's solutions, the unit channel conductance was ohmic and ranged from 22 to 33 pS (mean, 26.8 +/- 0.6 pS, n = 24). When NaCl was replaced by KCl (n = 8) or sodium gluconate (n = 2) on the cytoplasmic side of the membrane, single-channel currents still reversed at 0 mV and the conductance was unchanged. The reversal potential was +28.8 +/- 0.4 mV (n = 8) when a NaCl concentration (140 vs. 42 mmol/l) gradient was applied, close to the expected value (approx. 30 mV) for a cation selective channel. The channel was found to discriminate poorly between Na+, K+, Cs+, and Li+ ions. The activity of the channel was not clearly voltage-dependent but was dependent upon the free Ca2+ concentration on the cytoplasmic side of the membrane. We conclude that the channel resembles the non-selective cation channel which has been previously described in several tissues.

Animals↗
PubMed1969

Mechanism of exaggerated natriuresis in hypertensive man: impaired sodium transport in the loop of Henle.

To evaluate the effects of saline loading on distal sodium reabsorption in hypertensive man, studies were performed during both water deprivation and water diuresis in eight hypertensive subjects, and the results were compared to data obtained from similar studies in normal subjects. All hypertensive patients exhibited an enhanced excretion of filtered sodium (C(Na)/C(In)) at any level of distal delivery of sodium compared to normal controls. Free water reabsorption (T(c) (H2O)) during hypertonic saline loading was quantitatively abnormal in the hypertensives at high levels of osmolar clearance (C(Osm)), and also the curve of T(c) (H2O) vs. C(Osm) leveled off above a C(Osm) of 18 ml/min per 1.73 m(2) in the hypertensive group in contrast to the normal controls in whom T(c) (H2O) showed no evidence of achieving an upper limit. Sodium depletion exaggerated the abnormality in T(c) (H2O) in hypertensives, and resulted in a positive free water clearance (C(H2O)) during hydropenia. During hypotonic saline loading in water diuresis, changes in free water clearance per 100 ml of glomerular filtrate (C(H2O)/C(In)) were less at any given increment in urine flow per 100 ml of glomerular filtrate (V/C(In)) in the hypertensives compared to normal controls (P < 0.001). This abnormality in C(H2O)/C(In) in the hypertensives in conjunction with the defect in T(c) (H2O) observed during hydropenia indicates that sodium reabsorption in the loop of Henle was abnormal at any given rate of distal delivery of sodium in hypertension. Furthermore, these abnormalities in T(c) (H2O) and C(H2O) coincided temporally with the development of the exaggerated natriuresis. Although the distal defect in sodium transport, in large part, accounted for the augmented natriuresis in hypertension, evidence was present also for enhanced rejection of sodium in the proximal tubule during saline loading in the hypertensives. Additional studies utilizing acetazolamide which increases distal delivery of sodium without extracellular fluid volume expansion showed only minimal abnormalities in C(H2O) in the hypertensive group, indicating that the defect in sodium transport in the loop of Henle in hypertensives is mainly an abnormal response to extracellular fluid expansion rather than an intrinsic defect in the loop to handle increased tubular loads of sodium. It is possible that the abnormality in sodium reabsorption in the loop of Henle is due to the transmission of the abnormally elevated blood pressure of the hypertensives to the medullary vasa recta during saline loading.

Acetazolamide↗
PubMed1992

Active NaCl transport in the cortical thick ascending limb of Henle's loop of the mouse does not require the presence of bicarbonate.

The aim of the present study was to investigate whether bicarbonate buffer (CO2 + HCO3-) is required to sustain maximal NaCl transport in the cortical thick ascending limb of Henle's loop (cTAL) of the mouse. Transepithelial Na+ and Cl- net fluxes (JNa, JCl, pmol min-1 mm-1), measured by electron microprobe analysis, were similar irrespective of the presence or absence of CO2 + HCO3- in luminal and bathing solutions (JNaCl with CO2 + HCO3- = 203 +/- 25 pmol min-1 mm-1; JNaCl without CO2 + HCO3- = 213 +/- 13 pmol min-1 mm-1, n = 14). Furthermore the transepithelial potential difference, Vte, the transepithelial resistance, Rte, and the basolateral membrane potential, Vbl, were unaffected by CO2 + HCO3-. In the absence of CO2 + HCO3-, Vte was +17.0 +/- 1.7 mV (n = 9) (lumen positive), Rte was 28 +/- 2 omega cm2 (n = 9) and Vbl was -76 +/- 4 mV (n = 6). In the presence of CO2 + HCO3-, Vte, Rte and Vbl were +15.9 +/- 1.5 mV, 29 +/- 1 omega cm2 and -73 +/- 5 mV, respectively. 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulphonic acid (SITS; 0.1 mmol l-1) and amiloride (1 mmol l-1) added to the (CO2 + HCO3-)-containing lumen perfusate were without effect on Vte and Rte. Finally, the effect of furosemide (0.1 mmol l-1) on Vte and Vbl in the presence of CO2 + HCO3- was investigated. Furosemide reversibly decreased Vte from +13.7 +/- 1.1 mV to +1.7 +/- 0.7 mV (n = 6) and hyperpolarized Vbl from -70 +/- 1 to -89 +/- 3 mV (n = 5), suggesting passive distribution of Cl- across the basolateral membrane. In conclusion, these data suggest that active NaCl transport in the cTAL of the mouse does not require the presence of CO2 + HCO3-.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1989

Furosemide directly stimulates prostaglandin E2 production in the thick ascending limb of Henle's loop.

Studies were conducted to investigate direct effects of loop diuretics on prostaglandin E2 (PGE2) production using microdissected nephron segments. At first, the effect of indomethacin on the diuretic response to furosemide was re-evaluated in anesthetized rats. Indomethacin significantly attenuated the diuretic, natriuretic and chloruretic effects of furosemide without significantly affecting inulin and p-aminohippurate clearance or filtration fraction. But, in nondiuretic states, indomethacin had no significant effects on these parameters. Furosemide, ethacrynic acid and bumetanide significantly increased PGE2 production in cortical and medullary thick ascending limbs of Henle's loop (P less than .001), but not PGE2 production in the cortical and outer medullary collecting tubules. The effect of furosemide on PGE2 production in CTAL was dose-dependent, and higher concentrations of of furosemide than 10(-6) M significantly increased PGE2 production. On the other hand, chlorothiazide showed no PGE2 productive stimulation in these four nephron segments. This study demonstrates that the enhanced PGE2 production in the thick ascending limb of Henle's loop by furosemide and other loop diuretics is one possible mechanism of these drugs.

Animals↗
PubMed1984

Volume expansion modulates NaHCO3 and NaCl transport in the proximal tubule and Henle's loop.

The effects of extracellular fluid volume expansion on kidney reabsorption of bicarbonate, chloride, and water were examined in Sprague-Dawley rats by paired micropuncture experiments in which tubular fluid was collected from early distal and end-proximal sites. In group I, rats were studied during a plasma-replete euvolemic state and after 10% body wt colloid-free volume expansion. The filtered loads were similar in euvolemia and expansion; expansion increased end-proximal total CO2 concentration ([tCO2] EP) from 13.0 +/- 0.8 to 18.4 +/- 0.7 mM and inhibited the tCO2 fractional reabsorption 26% in the proximal convoluted tubule and 15% in Henle's loop. Early distal tCO2 delivery therefore increased from 61 +/- 7 to 140 +/- 17 pmol X min-1 X g kidney wt-1. A more pronounced inhibition of fractional reabsorption of chloride (45%) and water (35%) occurred in the proximal convoluted tubule during expansion. In group II, rats were studied during 5% body wt 70 g/liter albumin-containing expansion and after 10% body wt colloid-free expansion. Compared with euvolemia of group I, albumin expansion decreased proximal fractional reabsorption of tCO2 13%, chloride 19%, and water 14% without change in filtered loads, and [tCO2]EP rose to 17.2 +/- 0.7 mM. A 10 g/liter decrease in plasma protein concentration during colloid-free expansion was associated, compared with albumin expansion, with inhibition of proximal fractional reabsorption of tCO2 by 4%, chloride by 18%, and water by 9% without further altering [tCO2]EP. We conclude that 1) expansion specifically inhibits bicarbonate reabsorption in the proximal convoluted tubule and in Henle's loop independent of change in filtered load or in peritubular protein concentration, probably by enhancing bicarbonate backdiffusion and reducing proton secretion; 2) expansion-induced decrease in peritubular protein concentration contributes to the proximal expansion effect probably by specifically inhibiting transcellular sodium chloride reabsorption.

Animals↗
PubMed1983

Effect of acute potassium load on reabsorption in Henle's loop in the rat.

Rats fed a low potassium diet were studied before and after KCl infusion to determine whether potassium recycling in the renal medulla accelerates potassium excretion by increasing delivery of sodium, water, and potassium to the distal tubule. Fluid samples were obtained from the end-proximal and beginning-distal tubule before and at the same sites after KCl loading by re-collection micropuncture and were compared with samples obtained from similarly fed control animals not infused with KCl. Potassium excretion increased in the KCl group from 3 to 48% but remained low in the controls. Fractional sodium and water delivery to end-proximal and beginning-distal tubule increased with time equally in both groups. Potassium reabsorption in Henle's loop fell from 75 to 58% (P less than 0.005) after KCl infusion but not significantly in the controls (from 77 to 75%). Fractional potassium delivery to the distal tubule increased from 12 to 26% (P less than 0.005) in the KCl group, which could account for over half the potassium excreted. The increase in controls from 12 to 17% was significantly less (P less than 0.02). These findings suggest that potassium recycling reduces potassium reabsorption in Henle's loop, enabling the loop to participate with the distal and collecting tubule in accelerating urinary excretion of an acute potassium load.

Animals↗
PubMed1989

Protein intake and cation transport in the loop of Henle.

High-protein intake enhances maximal urinary concentrating ability and suppresses tubuloglomerular feedback activity in a manner that correlates with enhanced salt reabsorption in the loop of Henle. In this article we describe studies designed to localize the site at which protein intake alters loop sodium uptake (JNa) in rats fed diets containing either 6% or 40% protein for approximately 8 to 10 days. In vivo microperfusion demonstrated that luminal bumetanide (10(-5) mol/L) fully reversed the stimulation of JNa by high-protein intake, thus suggesting that high-protein intake stimulates salt transport in the thick ascending limb. In vitro studies supported this possibility, showing that high-protein intake significantly increased sodium-potassium adenosine triphosphatase (NaK ATPase) activity in homogenates of outer renal medulla (68%) and in dissected medullary thick ascending limbs (87%). This effect was partly selective, since high-protein intake did not alter NaK ATPase activity in superficial renal cortex, had a smaller and statistically insignificant effect on NaK ATPase activity in dissected pars rectae, and did not affect magnesium ATPase activity in any tissue. Furthermore, this effect did not appear to require hypertrophy, since high-protein intake for approximately 8 days did not detectably alter the relative amounts of tissue protein and DNA in either medulla or cortex. A last series of studies demonstrated that high-protein intake increased plasma aldosterone levels. We conclude that increased protein intake stimulates salt reabsorption predominantly in the thick ascending limb, an effect that is partly selective; does not appear to require hypertrophy; and may be related to increased plasma aldosterone levels.

Aldosterone↗
PubMed1993

Ammonium and bicarbonate transport in isolated perfused rodent ascending limbs of the loop of Henle.

Ammonium accumulates in the renal medullas of antidiuretic animals, presumably due to countercurrent multiplication, driven by NH4+ absorption from ascending loops of Henle in the outer and inner medulla. Active absorption of NH4+ occurs in the thick ascending limb (TAL). But the passive transport properties of NH3 in the TAL and the transport of ammonium or HCO3- in the ascending thin limb (ATL) have not been studied in rodents. To investigate the potential role of the ascending limb segments in medullary accumulation of ammonium, we perfused isolated subsegments of the chinchilla ATL and of the rat ATL and TAL. After imposing concentration gradients of total ammonia or total CO2 across ATL subsegments, we found very high rates of transfer of both substances, implying that at physiological flow rates the tubule luminal fluid quickly equilibrates with the interstitium. In the medullary TAL, we found a passive NH4+ permeability of 17 x 10(-5) cm/s but a relatively low NH3 permeability of < 0.003 cm/s. The low NH3 permeability prevents backleak of NH3 when NH4+ is actively transported from the lumen. We conclude that the ATL acts as an equilibrating segment and the TAL has special permeability properties that enhance net ammonium absorption and therefore enhance medullary ammonium accumulation.

Ammonia↗
PubMed1977

The transition of the thick ascending limb of Henle's loop into the distal convoluted tubule in the nephron of the rat kidney.

Examination of serial semithin sections of rat kidney cortex and a subsequent electron microscopic study of selected areas revealed that the characteristic epithelium of the cortical part of the thick ascending limb of Henle extends for a varying distance beyond the macula densa. The transition from the relatively thin epithelium of the thick ascending limb at this site to the three--or even four--fold thicker epithelium of the convoluted part of the distal tubule is sharply defined and occurs without the interposition of an intermediate cell type. The position of the macula densa at the end but still clearly within the ascending limb of Henle's loop is functionally interpreted to guarantee the separation of the sensor point macula densa from disturbing influences which might arise from the secretory activity of the subsequent tubular portion.

Animals↗
PubMed1989

A cation channel in the thick ascending limb of Henle's loop of the mouse kidney: inhibition by adenine nucleotides.

1. Patch-clamp single-channel current recordings were used to study the inhibition of Ca2+-activated non-selective cation channels by internal nucleotides in patches excised from basolateral membranes of the thick ascending limb of Henle's loop of the mouse kidney. 2. The application of ATP, ADP or AMP to the cytoplasmic face of excised inside-out membrane patches reduced the open-state probability of the channels (Po) in a dose-dependent way without effect upon the unitary current amplitude. Dose-response curves gave half-maximal inhibitory concentrations of 20, 21 and 2.5 microM for ATP, ADP and AMP, respectively, while the Hill coefficient was close to one in all three cases. 3. Cyclic AMP partially inhibited channel activity (Po = 35 +/- 17% of control) only at high, unphysiological concentrations (10(-3) M) while adenosine (10(-3) M) had very little effect (Po = 83 +/- 7% of control). 4. Replacement of adenine with other purines (guanine, hypoxanthine) or pyrimidine (uridine) bases very largely reduced inhibitory activity. Cyclic GMP had no effect. 5. Non-hydrolysable analogues of ATP, AMP-PNP (10(-3) M) and ATP-gamma-S (5 x 10(-4) M), were effective inhibitors of the channel (Po = 24 +/- 7 and 9 +/- 4% of control, respectively.

Adenine Nucleotides↗
PubMed1980

Lithium-induced polyuria: effect of lithium on adenylate cyclase and adenosine 3',5'-monophosphate phosphodiesterase in medullary ascending limb of Henle's loop and in medullary collecting tubules.

We investigated the effects of hyperosmolality, chronic treatment with lithium chloride (LiCl), and the addition of LiCl in vitro on vasopressin-sensitive (VP) adenylate cyclase (AdC) and cAMP phosphodiesterase (cAMP-PDIE) activities in the medullary thick ascending limb of Henle's loop (MAL) and medullary collecting tubule (MCT) microdissected from the outer medulla of the rat kidney. A hyperosmolar medium (800 mosmol) markedly enhanced AdC activity stimulated by 10(-6) M VP specifically in MCT, while having little effect or slightly decreasing VP-stimulated AdC in MAL, compared to activities under standard isotonic conditions. Hyperosmolality decreased cAMP-PDIE activity to about the same degree in MAL and MCT. Inclusion of LiCl in the incubation medium (15-20 mM) caused a significant dose-dependent inhibition of VP-stimulated AdC activity in both MAL and MCT, but had no effect on CAMP-PDIE in either segment. AdC and cAMP-PDIE activities in MAL and MCT from chronic LiCl-treated polyuric rats did not differ from controls when assayed under standard isotonic conditions. However, when assayed in a hyperosmolar (800 mosmol) medium, VP-sensitive AdC activity was significantly lower (P < 0.01) in MCT from LiCl-treated rats compared to control levels, while VP-sensitive AdC in MAL did not differ in LiCl-treated and control rats. The present results suggest that lowered VP-sensitive AdC activity in MCT of LiCl-treated polyuric rats may contribute to the observed lower concentrating ability and collecting tubule resistance to VP. Inhibition of VP-sensitive AdC in MAL as well as MCT by the acute addition of LiCl in vitro may explain the decreased urinary diluting ability observed with acute infusions of Li salts in vivo in the rat.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1984

PTH-like glucagon stimulation of Ca and Mg reabsorption in Henle's loop of the rat.

The effects of glucagon and PTH on renal tubular electrolyte handling were studied in anesthetized, thyroparathyroidectomized Brattleboro rats infused with somatostatin. Fractional excretion of Ca and Mg was significantly lower during infusion of both hormones. Micropunctures of same nephrons localized the bulk of the increase in reabsorption in Henle's loop, where both hormones significantly enhanced the reabsorptive capacities for Ca, Mg, and K. Beyond the early distal tubule, Ca and Mg reabsorption was significantly greater during glucagon infusion and Ca reabsorption was significantly greater during PTH infusion. Cyclic adenosine monophosphate at a plasma concentration of 10(-6) M did not reproduce the effects of either glucagon or PTH. These results are similar to the findings reported for the effects of ADH and calcitonin on Ca, Mg, and K tubular handling, but different as far as Na and Cl are concerned, since their loop reabsorption was not significantly altered by glucagon and PTH. The data obtained here for glucagon and PTH, together with those for ADH and calcitonin, support the hypothesis that these four hormones exert similar effects in the thick ascending limb.

Absorption↗
PubMed1990

Effects of antidiuretic hormone, parathyroid hormone and glucagon on transepithelial voltage and resistance of the cortical and medullary thick ascending limb of Henle's loop of the mouse nephron.

The effect of antidiuretic hormone (arginine vasopressin, AVP, 10(-10) mol.l-1), parathyroid hormone (PTH, 10(-8) mol.l-1) and glucagon (10(-8) mol.l-1) on the transepithelial potential difference (PDte) and the transepithelial resistance (Rte) were tested in in vitro perfused cortical (cTAL) and medullary (mTAL) thick ascending limbs of Henle's loop of the mouse nephron. When compared with mTAL segments (PDte: 8.5 +/- 0.4 mV, n = 16), cTAL segments displayed a high PDte of 15.7 +/- 0.9 mV (n = 11) at the beginning of perfusion experiments which reached a value of 9.4 +/- 0.6 mV (n = 11) after 38 +/- 4 min perfusion. Simultaneously Rte increased significantly from 24 +/- 3 to 28 +/- 1 omega cm2 (n = 11). When PTH, AVP or glucagon were added to the bath solution, PDte increased with PTH from 10.3 +/- 0.8 to 15.2 +/- 0.8 mV (n = 13), with AVP from 10.2 +/- 0.5 to 15.0 +/- 0.7 mV (n = 24) and with glucagon from 11.3 +/- 1.9 to 15.3 +/- 2.1 mV (n = 8). At the same time Rte decreased from 30 +/- 3 to 23 +/- 2 omega cm2, from 28 +/- 1 to 23 +/- 1 omega cm2 and from 23 +/- 2 to 18 +/- 2 omega cm2, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Cytokines affect ion transport in primary cultured thick ascending limb of Henle's loop cells.

Tumor necrosis factor-alpha (TNF) and interleukin-1 (IL-1) affect epithelial cell ion transport. However, the site of action along the nephron has not been elucidated fully for these cytokines. Thus, the effect of TNF and IL-1 on the ion transport function of primary cultured medullary thick ascending limb of Henle's loop (mTALH) cells was determined by measuring rubidium (86Rb) uptake. TNF, IL-1, and lipopolysaccharide (LPS), a known activator of cytokine production, inhibited 86Rb uptake by cultured mTALH cells after a 24-h incubation period but had no effect when incubated with the cells for 1 or 4 h. Furthermore, mTALH cells produced biologically active TNF after stimulation with LPS for 24 h, and the LPS-induced inhibition of 86Rb uptake was abolished in the presence of an anti-TNF antibody, suggesting that TNF produced by the mTALH cells acted in an autocrine manner to inhibit 86Rb uptake. The effects of LPS on 86Rb uptake also were inhibited by the cyclooxygenase inhibitor, indomethacin. As TNF increased prostaglandin E2 synthesis by cultured mTALH cells and as prostaglandin E2 also inhibited 86Rb uptake, LPS presumably inhibited 86Rb uptake by inducing a TNF-mediated increase in prostaglandin synthesis. These data demonstrate that a prostanoid produced by mTALH cells mediates the inhibitory effect of LPS and TNF on 86Rb uptake and imply that endogenous TNF inhibits ion fluxes in the mTALH via a prostaglandin-dependent mechanism.

Animals↗