Effect of ADH on chloride reabsorption in the loop of Henle of the Brattleboro rat

1985 ◽  
Vol 249 (5) ◽  
pp. F698-F703 ◽  
Author(s):  
J. Work ◽  
J. H. Galla ◽  
B. B. Booker ◽  
J. A. Schafer ◽  
R. G. Luke
Keyword(s):  
Distal Tubule ◽  
Thick Ascending Limb ◽  
Brattleboro Rat ◽  
In Vitro Perfusion ◽  
Chloride Flux ◽  
Medullary Thick Ascending Limb ◽  
Transepithelial Voltage ◽  
Tubule Fluid

Both in vivo superficial loop segment microperfusion and in vitro perfusion of isolated medullary thick ascending limb segments were used to assess the effect of vasopressin on loop of Henle chloride absorption in the Brattleboro rat. Superficial loop segments were perfused between the latest proximal and earliest distal tubule in vivo at 19.2 +/- 0.4 nl/min (mean +/- SE) with an artificial tubule fluid. Under control conditions, absolute chloride reabsorption was 1,596 +/- 61 pmol/min and increased to 1,876 +/- 102 after intravenous infusion of vasopressin (P less than 0.005). Distal tubule fluid chloride concentration decreased 4.6 +/- 1.5 meq/liter (P less than 0.05), and fractional chloride reabsorption increased 4.8 +/- 2.0% (P less than 0.05). For in vitro perfusion, medullary thick ascending limb segments were bathed and perfused (9-15 nl/min) with phosphate-buffered solutions at 38 degrees C. Under control conditions, transepithelial voltage was +2.4 +/- 0.3 mV, lumen positive, and the net chloride flux was 147 +/- 24 pmol X min-1 X mm-1 in the absorptive direction. Addition of vasopressin to the bathing solution increased net chloride reabsorption to 342 +/- 56 pmol X min-1 X mm-1 (P less than 0.02) and transepithelial voltage to 3.0 +/- 0.3 mV (P less than 0.002). An additional group of tubules was examined under identical conditions; however, vasopressin was removed from the bathing medium during a subsequent recovery period. In these experiments, net chloride flux and transepithelial voltage significantly increased compared with the control period and returned to control values upon removal of vasopressin from the bath.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Angiotensin II inhibits NaCl absorption in the rat medullary thick ascending limb

2004 ◽  
Vol 287 (3) ◽  
pp. F404-F410 ◽  
Author(s):  
Nicolas Lerolle ◽  
Soline Bourgeois ◽  
Françoise Leviel ◽  
Gaëtan Lebrun ◽  
Michel Paillard ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Membranes ◽  
Inhibitory Effect ◽  
Thick Ascending Limb ◽  
Sprague Dawley ◽  
Experimental Conditions ◽  
Nacl Absorption ◽  
Medullary Thick Ascending Limb

NaCl reabsorption in the medullary thick ascending limb of Henle (MTALH) contributes to NaCl balance and is also responsible for the creation of medullary interstitial hypertonicity. Despite the presence of angiotensin II subtype 1 (AT1) receptors in both the luminal and the basolateral plasma membranes of MTALH cells, no information is available on the effect of angiotensin II on NaCl reabsorption in MTALH and, furthermore, on angiotensin II-dependent medullary interstitial osmolality. MTALHs from male Sprague-Dawley rats were isolated and microperfused in vitro; transepithelial net chloride absorption ( JCl) as well as transepithelial voltage ( Vte) were measured. Luminal or peritubular 10−11 and 10−10 M angiotensin II had no effect on JCl or Vte. However, 10−8 M luminal or peritubular angiotensin II reversibly decreased both JCl and Vte. The effect of both luminal and peritubular angiotensin II was prevented by the presence of losartan (10−6 M). By contrast, PD-23319, an AT2-receptor antagonist, did not alter the inhibitory effect of 10−8 M angiotensin II. Finally, no additive effect of luminal and peritubular angiotensin II was observed. We conclude that both luminal and peritubular angiotensin II inhibit NaCl absorption in the MTALH via AT1 receptors. Because of intrarenal angiotensin II synthesis, angiotensin II concentration in medullary tubular and interstitial fluids may be similar in vivo to the concentration that displays an inhibitory effect on NaCl reabsorption under the present experimental conditions.

Stimulation of distal potassium secretion by low lumen chloride in the presence of barium

1985 ◽  
Vol 248 (5) ◽  
pp. F638-F649 ◽  
Author(s):  
D. H. Ellison ◽  
H. Velazquez ◽  
F. S. Wright
Keyword(s):  
Chloride Concentration ◽  
Distal Tubule ◽  
Perfusion Fluid ◽  
Transport Pathway ◽  
Luminal Membrane ◽  
Potassium Secretion ◽  
Transepithelial Voltage ◽  
Tubule Fluid ◽  
Stimulation Of

Potassium secretion into the renal distal tubule is increased when chloride in the tubule fluid is replaced by another anion. The present experiments were done to determine whether this increment in transported potassium traverses a conductive pathway from cell to lumen. Transport rates of potassium, sodium, chloride, and fluid by the renal distal tubule of rats were examined in vivo by continuous microperfusion. The effects of substituting gluconate for chloride in the presence and absence of 5 mM barium in the perfusion fluid were determined. When gluconate replaced chloride in the perfusion solutions, potassium secretion increased (by 44%) without a significant change in transepithelial voltage. Barium in the lumen increased the magnitude of the lumen-negative transepithelial voltage (by 30%) and reduced potassium secretion (by 56%) by inhibiting conductive potassium movement. Barium also decreased both sodium (by 51%) and chloride (by 37%) absorption. Barium did not reduce the stimulation of potassium secretion caused by reducing lumen chloride concentration. Potassium secretion increased (by 77%) when lumen chloride was reduced in the presence of 5 mM barium. We interpret these results by postulating that a cotransport mechanism linking potassium and chloride is present in the luminal membrane of distal tubule cells, that this mechanism operates in parallel with a conductive transport pathway for potassium, and that the K-Cl cotransport mechanism is not inhibited by barium.

Basolateral membrane Cl−-, Na+-, and K+-coupled base transport mechanisms in rat MTALH

2002 ◽  
Vol 282 (4) ◽  
pp. F655-F668 ◽  
Author(s):  
Soline Bourgeois ◽  
Sandrine Massé ◽  
Michel Paillard ◽  
Pascal Houillier
Keyword(s):  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
Thick Ascending Limb ◽  
Transport Mechanisms ◽  
Medullary Thick Ascending Limb ◽  
Bilateral Absence ◽  
Transepithelial Voltage ◽  
Intracellular Alkalinization ◽  
Cellular Acidification

Mechanisms involved in basolateral HCO[Formula: see text] transport were examined in the in vitro microperfused rat medullary thick ascending limb of Henle (MTALH) by microfluorometric monitoring of cell pH. Removing peritubular Cl− induced a cellular alkalinization that was inhibited in the presence of peritubular 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS) and blunted in the absence of external CO2/HCO[Formula: see text]. The alkalinization elicited by removing peritubular Cl−persisted in the bilateral absence of Na+, together with a voltage clamp. When studied in Cl−-free solutions, lowering peritubular pH induced a base efflux that was inhibited by peritubular DIDS or by the absence of external CO2/HCO[Formula: see text]. Removing peritubular Na+ elicited a cellular acidification that was accounted for by stimulation of a DIDS- and ethylisopropylamiloride (EIPA)-insensitive Na+-HCO[Formula: see text] cotransport and inhibition of a basolateral Na+/H+exchange. Increasing bath K+ induced an intracellular alkalinization that was inhibited in the absence of external CO2/HCO[Formula: see text]. At 2 mM, peritubular Ba2+, which inhibits the K+-Cl−cotransport, did not induce any change in transepithelial voltage but elicited a cellular alkalinization and inhibited K+-induced cellular alkalinization, consistent with the presence of a basolateral, electroneutral Ba2+-sensitive K+-Cl− cotransport that may operate as a K+-HCO[Formula: see text] cotransport. This cotransport was inhibited in the peritubular presence of furosemide, [(dihydroindenyl)oxy]alkanoic acid, 5-nitro-2-(3-phenylpropylamino)benzoate, or DIDS. At least three distinct basolateral HCO[Formula: see text] transport mechanisms are functional under physiological conditions: electroneutral Cl−/HCO[Formula: see text] exchange, DIDS- and EIPA-insensitive Na+-HCO[Formula: see text] cotransport, and Ba2+-sensitive electroneutral K+-Cl−(HCO[Formula: see text]) cotransport.

Effect of PTH on calcium transport across the cortical thick ascending limb of Henle's loop

1980 ◽  
Vol 239 (2) ◽  
pp. F121-F126 ◽  
Author(s):  
J. E. Bourdeau ◽  
M. B. Burg
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Calcium Absorption ◽  
Calcium Flux ◽  
Thick Ascending Limb ◽  
Henle's Loop ◽  
Transepithelial Voltage ◽  
Net Flux ◽  
Stimulation Of

Cortical thick ascending limbs of Henle's loop were dissected from rabbit kidneys and perfused in vitro. Unidirectional transepithelial calcium fluxes from lumen-to-bath and bath-to-lumen were measured with 45Ca. The tubules were bathed in 150 mM sodium and perfused with 60 mM sodium to simulate conditions in the cortical thick ascending limb in vivo. During the 20-30 min preceding the addition of parathyroid hormone (PTH), net calcium absorption decreased from 0.207 to 0.084 pmol x s-1 x cm-1. After addition of synthetic bovine PTH (60-64 nM) to the bath, there was an immediate increase in calcium absorption, and by 20 min the net flux increased to 0.415 pmol x s-1 x cm-1. The increase in calcium absorption was due to an increase in the lumen-to-bath flux. Dibutyryl-cAMP or 8-BrcAMP mimicked PTH; adrenocorticotropic hormone had no effect on the calcium flux. Transepithelial voltage was unchanged after addition of PTH. We conclude that PTH increases calcium absorption across the cortical thick ascending limb, probably by stimulation of adenylate cyclase.

Ammonia and bicarbonate transport by thick ascending limb of rat kidney

1984 ◽  
Vol 247 (1) ◽  
pp. F35-F44 ◽  
Author(s):  
D. W. Good ◽  
M. A. Knepper ◽  
M. B. Burg
Keyword(s):  
Fluid Transport ◽  
Rat Kidney ◽  
Renal Medulla ◽  
Ammonia Concentration ◽  
Bicarbonate Transport ◽  
Thick Ascending Limb ◽  
Transepithelial Voltage ◽  
Ammonia Absorption ◽  
Tubule Fluid

Ammonia and bicarbonate transport by the thick ascending limb of rat kidney was studied to determine whether this segment contributes to the regulation of renal ammonia and net acid excretion. Cortical and medullary thick ascending limbs were perfused in vitro at 1.0-1.5 nl X min-1 X mm-1 with HCO3-buffered solutions. There was no significant net fluid transport. With 4 mM ammonia in bath and perfusate, transepithelial voltage averaged 6-9 mV, lumen positive, and did not differ between the two segments. The mean ammonia concentration in collected tubule fluid was 2.8 mM with cortical segments and 2.3 mM with medullary segments, indicating net absorption of ammonia. Furosemide (10(-4) M) in the perfusate eliminated ammonia absorption in medullary thick ascending limbs and converted net absorption to net secretion in cortical thick ascending limbs. Furosemide reduced transepithelial voltage to near zero in every tubule. Cortical and medullary thick ascending limbs also absorbed bicarbonate, indicating that their tubule fluid was acidified relative to the bath. Therefore, absorption of ammonia could not have occurred by nonionic diffusion. The absorption most likely was due to direct transport of NH4+. The possible mechanisms involved are discussed, and it is proposed that absorption of ammonia by thick ascending limbs provides a source for its accumulation in the renal medulla and secretion into the collecting ducts.

Transepithelial HCO3− absorption is defective in renal thick ascending limbs from Na+/H+ exchanger NHE1 null mutant mice

2004 ◽  
Vol 287 (6) ◽  
pp. F1244-F1249 ◽  
Author(s):  
David W. Good ◽  
Bruns A. Watts ◽  
Thampi George ◽  
Jamie W. Meyer ◽  
Gary E. Shull
Keyword(s):  
Rat Kidney ◽  
Basolateral Membrane ◽  
Thick Ascending Limb ◽  
Wild Type ◽  
Medullary Thick Ascending Limb ◽  
Transepithelial Voltage ◽  
Regulatory Defect ◽  
Null Mutant Mice

In the medullary thick ascending limb (MTAL) of rat kidney, inhibiting basolateral Na+/H+ exchange with either amiloride or nerve growth factor (NGF) results secondarily in inhibition of apical Na+/H+ exchange, thereby decreasing transepithelial HCO3− absorption. To assess the possible role of the Na+/H+ exchanger NHE1 in this regulatory process, MTALs from wild-type and NHE1 knockout (NHE1−/−) mice were studied using in vitro microperfusion. The rate of HCO3− absorption was decreased 60% in NHE1−/− MTALs (15.4 ± 0.5 pmol·min−1·mm−1 wild-type vs. 6.0 ± 0.5 pmol·min−1·mm−1 NHE1−/−). Transepithelial voltage, an index of the NaCl absorption rate, did not differ in wild-type and NHE1−/− MTALs. Basolateral addition of 10 μM amiloride or 0.7 nM NGF decreased HCO3− absorption by 45–49% in wild-type MTALs but had no effect on HCO3− absorption in NHE1−/− MTALs. Inhibition of HCO3− absorption by vasopressin and stimulation by hyposmolality, both of which regulate MTAL HCO3− absorption through primary effects on apical Na+/H+ exchange, were similar in wild-type and NHE1−/− MTALs. Thus the regulatory defect in NHE1−/− MTALs is specific for factors (bath amiloride and NGF) shown previously to inhibit HCO3− absorption through primary effects on basolateral Na+/H+ exchange. These findings demonstrate a novel role for NHE1 in transepithelial HCO3− absorption in the MTAL, in which basolateral NHE1 controls the activity of apical NHE3. Paradoxically, a reduction in NHE1-mediated H+ extrusion across the basolateral membrane leads to a decrease in apical Na+/H+ exchange activity that reduces HCO3− absorption.

Ischemia-reperfusion induces G-CSF gene expression by renal medullary thick ascending limb cells in vivo and in vitro

2004 ◽  
Vol 286 (6) ◽  
pp. F1193-F1201 ◽  
Author(s):  
Ying Zhang ◽  
Vanessa K. Woodward ◽  
John M. Shelton ◽  
James A. Richardson ◽  
Xin J. Zhou ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Ischemia Reperfusion ◽  
Inflammatory Cells ◽  
Thick Ascending Limb ◽  
Rnase Protection ◽  
Medullary Thick Ascending Limb ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony

Ischemic acute renal failure involves not only the kidney but also extrarenal organs such as the bone marrow that produces inflammatory cells. By ELISA and RNase protection assays, we now show that renal ischemia-reperfusion increases serum concentrations of granulocyte macrophage colony-stimulating factor (G-CSF) protein and increases both G-CSF mRNA and protein in the ischemic kidney. In situ hybridization localized the increased G-CSF mRNA to tubule cells, including medullary thick ascending limb cells (mTAL), in the outer medulla. We also show that mTAL produce G-CSF protein and increase G-CSF mRNA after stimulation by reactive oxygen species in vitro. The production of G-CSF by the kidney after ischemia-reperfusion provides a means of communication from the injured kidney to the bone marrow. This supports the known inflammatory response to ischemia.

Endogenous nitric oxide inhibits chloride transport in the thick ascending limb

1999 ◽  
Vol 276 (1) ◽  
pp. F159-F163 ◽  
Author(s):  
Craig F. Plato ◽  
Barbara A. Stoos ◽  
Ding Wang ◽  
Jeffrey L. Garvin
Keyword(s):  
Nitric Oxide ◽  
Chloride Transport ◽  
Thick Ascending Limb ◽  
Chloride Flux ◽  
Nacl Transport ◽  
No Donor ◽  
Endogenous Nitric Oxide ◽  
Spermine Nonoate

Nitric oxide (NO) inhibits transport in various nephron segments, and the thick ascending limb of the loop of Henle (TALH) expresses NO synthase (NOS). However, the effects of NO on TALH transport have not been extensively studied. We hypothesized that endogenously produced NO directly decreases NaCl transport by the TALH. We first determined the effect of exogenously added NO on net chloride flux ( J Cl). The NO donor spermine NONOate (SPM; 10 μM) decreased J Cl from 101.2 ± 9.6 to 65.0 ± 7.7 pmol ⋅ mm−1 ⋅ min−1, a reduction of 35.5 ± 6.4%, whereas controls did not decrease over time. To determine whether endogenous NO affects cortical TALH transport, we measured the effect of adding the NOS inhibitor N G-nitro-l-arginine methyl ester (l-NAME), the substratel-arginine (l-Arg), or its enantiomerd-arginine (d-Arg) on J Cl.l-NAME andd-Arg did not alter J Cl; in contrast, addition of 0.5 mM l-Arg decreased J Cl by 40.2 ± 10.4% from control. The inhibition of chloride flux by 0.5 mM l-Arg was abolished by pretreatment with l-NAME, indicating that cortical TALH NOS is active, but production of NO is substrate-limited in our preparation. Furthermore, cortical TALH chloride flux increased following removal of 0.5 mMl-Arg from the bath, indicating that the reductions in chloride flux observed in response tol-Arg are not the result of NO-mediated cytotoxicity. We conclude that 1) exogenous NO decreases cortical TALH J Cl; 2) cortical TALHs produce NO in the presence of l-Arg, which decreases J Cl; and 3) the response of cortical TALHs to l-Arg is reversible in vitro. These data suggest an important role for locally produced NO, which may act via an autocrine mechanism to directly affect TALH sodium chloride transport. Thus TALH NO synthesis and inhibition of chloride transport may contribute to the diuretic and natriuretic effects of NO observed in vivo.

Diluting segment in avian kidney. I. Characterization of transepithelial voltages

1986 ◽  
Vol 250 (3) ◽  
pp. R333-R340 ◽  
Author(s):  
H. Nishimura ◽  
M. Imai ◽  
M. Ogawa
Keyword(s):  
Close Contact ◽  
Distal Tubule ◽  
Renal Tubules ◽  
Thick Ascending Limb ◽  
Diluting Segment ◽  
Cyanide Bath ◽  
Avian Kidney ◽  
Transepithelial Voltage

Renal tubules from the Japanese quail, Coturnix coturnix, were perfused in vitro to characterize the transepithelial voltage (Vt). The thick limb (TL) of the mammalian-type (MT) nephron showed Vt positive in the lumen (+9.1 +/- 0.7 mV, n = 35). The Vt decreased with increases in hydrostatic perfusion pressure. Furosemide (lumen), Na cyanide (bath), and ouabain (bath) reversibly reduced Vt. Removal of Cl or Na from the perfusate and the bath decreased Vt of the TL from +10.3 +/- 3.0 to -0.3 +/- 0.3 (n = 5) and from +7.4 +/- 1.5 to +1.2 +/- 0.2 mV (n = 8), respectively. The distal tubule of the reptilian-type (RT) nephron showed two types of Vt: a lumen-negative Vt in the late segment and a lumen-positive Vt in the early segment that is in close contact with the parent glomerulus. Both voltages were reversibly reduced by ouabain and Na cyanide. These results suggest that in quail the TL of the MT nephron resembles the thick ascending limb of the mammalian kidney with both Na and Cl required for generation of luminal positivity and the distal tubule of the RT nephron appears functionally heterogeneous.

Action of ADH on isolated medullary thick ascending limb of the Brattleboro rat

1986 ◽  
Vol 251 (2) ◽  
pp. F271-F277 ◽  
Author(s):  
K. Besseghir ◽  
M. E. Trimble ◽  
L. Stoner
Keyword(s):  
Chronic Administration ◽  
Osmotic Gradient ◽  
Thick Ascending Limb ◽  
Nacl Transport ◽  
Medullary Thick Ascending Limb ◽  
Gradual Process ◽  
Rapid Effect

Establishment of a maximal corticomedullary osmotic gradient during chronic administration of arginine vasopressin (antidiuretic hormone, ADH) to Brattleboro (diabetes insipidus, DI) rats is a gradual process. The effects of ADH on voltage and radioisotopic chloride efflux (lumen to bath) were investigated in medullary thick ascending limb (mTAL) isolated from DI rats and perfused in vitro. Acute in vitro exposure of mTAL to ADH (250 microU/ml) significantly increased both the voltage (+3.3 +/- 0.3 to +4.5 +/- 0.5 mV) and chloride efflux (192.7 +/- 29.4 to 240.4 +/- 41.5 peq/min X mm). After chronic in vivo treatment with ADH for 10-21 days mTAL expressed substantially higher basal voltage and chloride efflux (+8.4 +/- 0.6 mV and 393.2 +/- 71.6 peq/min X mm). Acute in vitro application of ADH to mTAL from chronically treated animals induced a further small increase in voltage (22%). These results are taken to indicate that ADH may have dual effects on NaCl transport by the mTAL of the DI rat: a small rapid effect, and a larger long-term increase in transport that can be shown only after chronic administration of ADH. These effects may, in part, explain the gradual enhancement of concentrating ability observed in DI rats.

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