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PubMed1978

[Ion excretion by the rat kidney in depressed reabsorption in proximal tubule and ascending protion of the loop of Henle].

Simultaneous suppression of reabsorption in the proximal tubule with the aid of polyethylenglucole 400 (PEG) and in ascending part of Henle's loop with furosemide increased diuresis by 121 times and natri-uresis by 242 times on the average. The increase was based on changes in the tubule reabsorption and secretion. The changes of sodium and calcium excretion as well as excretion of potassium and magnesium were parallel. Excretion of sodium and calcium was lesser than the diuresis while that of magnesium and potassium exceeded it. Furosemide reduced the reabsorption of osmotically free water.

Absorption↗
PubMed1983

[The osmoregulating function of the kidney and activity of the loop of Henle in water rats, gerbils and Brattleboro rats].

The concentration index U-P Osm in dehydration was 7.9 in gerbil, 2.7 in water rats and 1.7 in the Brattleboro homozygote rats. The sodium content in the kidney medullar substance of the animals under study correlated with the ability for creation of the high concentration gradient U-P Osm. The sodium excretion for 100 ml of filtrate, in maximal suppression with furosemide of the Cl- ions reabsorption in the large ascending parti of Henle's loop, was practically the same in all the rodents under study. This suggests that not only the amount of reabsorbed sodium but also the morpho-functional organization of the kidney medullar substance aiding to retainment of sodium, maintain the creation of high osmotic gradient.

Animals↗
PubMed1983

Distribution of filipin-sterol complexes in plasma membranes of the kidney. II. The thin limbs of Henle's loop.

Thin limbs of Henle from the rat kidney were investigated by freeze fracture electron microscopy after incubation of the tissue with the polyene antibiotic, filipin, a morphologic probe for membrane cholesterol. Distinct patterns of distribution of filipin-sterol complexes were found in plasma membranes of epithelial cells from each of the four thin limb regions examined. In particular, adjacent cells in the thin ascending limb had either heavily or poorly labeled apical membranes, whereas in the lower part of long descending thin limbs, all apical membranes were poorly labeled. In contrast, both apical and basolateral membranes of short descending limbs were heavily labeled with filipin-sterol complexes. These results demonstrate the existence of plasma membranes with different properties both within specific segments of Henle's loop (ascending thin limb) and between different thin limb segments (short and long descending limbs).

Animals↗
PubMedDate not supplied

Bicarbonate transport along the loop of Henle: molecular mechanisms and regulation.

The loop of Henle (LOH) is an important site of renal tubule acidification. A combination of several techniques, including in vivo microperfusion, perfusion in vitro of the S3 segment of the proximal tubule and of the thick ascending limb (TAL) of Henle's loop, as well as quantitative PCR performed on isolated TAL, has permitted the definition of key transporters and their role in modulating bicarbonate reabsorption in physiological and pathophysiological conditions. Na(+)-H+ exchange is the most important transport mechanism responsible for bicarbonate reabsorption, although a small but significant contribution of H(+)-ATPase-mediated bicarbonate reabsorption can also be identified. NHE3 is the main of several NHE isoforms expressed in the TAL and in the S3 segment of the proximal tubule. Special properties of the Na(+)-H+ exchanger in the TAL are its relative insensitivity to changes in cell pH (pHi) and the tight coupling between apical and basolateral Na(+)-H+ exchange. Several hormones, including anti-diuretic hormone (ADH), angiotensin II (AII), and gluco- and mineralocorticoids regulate Na(+)-H+ exchange. Loop diuretics such as furosemide stimulate bicarbonate transport along the LOH. Systemic acid-base disturbances also modulate bicarbonate transport: acidosis increases bicarbonate reabsorption, while metabolic alkalosis has the opposite effect. Neither hypokalemic alkalosis nor respiratory alkalosis or respiratory acidosis alter bicarbonate transport along the LOH. A significant role of HCO3 backflux, most likely through the paracellular pathway of the TAL, can also be observed. Changes in extracellular osmolality also affect bicarbonate reabsorption: hypertonicity inhibits, whereas hypotonicity stimulates transport. Transport activation is also observed as an adaptive response to glomerular hyperfiltration.

Absorption↗
PubMed2003

Analysis of energy metabolism and mechanism of loop diuretics in the thick ascending limb of Henle's loop in dog kidneys.

AIM: The thick ascending limb of Henle's loop (TALH) absorbs up to 40% of filtered NaCl in volume-expanded dogs. To examine if a fraction of this absorption is passive, NaHCO3 absorption and associated NaCl absorption in proximal tubules were inhibited by acetazolamide, a carbonic anhydrase inhibitor. RESULTS: Ouabain, a specific inhibitor of Na,K-ATPase activity, reduced the remaining NaCl absorption and renal oxygen consumption in a ratio DeltaNa/DeltaO2 = 18, as expected for active transport. However, the responses to two loop diuretics were DeltaNa/DeltaO2 = 24 for ethacrynic acid and DeltaNa/DeltaO2 = 30 for bumetanide. Both loop diuretics induced potassium secretion. By superimposing ouabain potassium secretion was stopped and DeltaNa/DeltaO2 = 18 restored. Replacement of half of the circulating NaCl with Na2SO4 gave stop-flow pattern similar to those obtained after ethacrynic acid. CONCLUSIONS: Low entry of some sodium ions thorugh the apical membrane is permitted despite low chloride supply or blockade by loop diuretics of chloride entry by the Na-K-2Cl transporter. Continued Na-K-ATPase activity causes secretion of potassium ions through the apical ion channel, ethacrynic acid being more kaliuretic and less natriuretic than bumetanide. Greater paracellular recycling of sodium ions after bumetanide maintains ionic balance. In contrast, under normal conditions excess entry of chloride by the Na-K-2Cl-transporter leads to paracellular back-diffusion of chloride rather than paracellular absorption of sodium ions, consistent with DeltaNa/DeltaO2 = 18 after ouabain. Thus all NaCl transport along TALH is active in vivo, whereas absorption of other cations, such as lithium, probably is passive.

Absorption↗
PubMed1982

Thick ascending limb of Henle's loop.

Thick ascending limbs of Henle's loop have at least three major roles: (1) They reabsorb sodium chloride which dilutes the urine. (2) The reabsorption of sodium chloride also produces concentration gradients that drive the countercurrent multiplier system in the medulla and medullary rays and thus concentrates the urine. (3) They reabsorb large amounts of potassium, calcium, and magnesium in an energy-efficient manner. The mechanisms involved in these functions are reviewed in this paper, emphasizing the results of direct studies on isolated tubule segments.

Aldosterone↗
PubMed1979

Voltage dependence of calcium transport in the thick ascending limb of Henle's loop.

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 using different solutions that caused the transepithelial voltage to vary over a wide range. With lumen-positive voltages there was net calcium absorption from lumen to bath which varied directly with the voltage. With voltage near zero there was no measurable net flux. When the voltage was made negative, the direction of net calcium transport reversed (i.e., secretion from bath to lumen). The presence or absence of bicarbonate in the lumen did not affect the calcium fluxes. Calcium permeability, calculated from the dependence of net flux on voltage, was 7.7 x 10(-6) cm/s, which is approximately 25% of the sodium permeability previously determined in this segment. Analysis of the calcium flux ratios revealed interdependence of the bidirectional fluxes consistent with single-file diffusion but no evidence for active calcium transport. We conclude that there is an important component of passive net calcium transport driven by the voltage in this segment.

Animals↗
PubMed1990

Ionic dependence of cell volume regulation by the thin ascending limb of Henle's loop.

Thin ascending limb cells from Henle's loop were studied with optical and video techniques to evaluate cell volume regulation in response to anisoosmotic media and its ionic dependence. Cell volume regulation was observed when these cells were exposed to hypoosmotic solutions. Under hyperosmotic conditions only an osmometric response was found, with no volume regulatory increase (VRI). The removal of Cl- or HCO3- abolished the volume regulatory decrease (VRD) normally observed during exposure to hypoosmotic solutions. Re-addition of these ions did not elicit the VRD response. The removal of K+ from hypoosmotic solutions abolished VRD but its re-introduction restored the volume regulatory response. In the absence of Na+, a partial inhibition of VRD was found; re-addition of Na+ completely restored the regulatory response. These indicate that cells from the thin ascending limb of Henle's loop regulate their volume under hypoosmotic conditions, and that this process is dependent upon Cl-, HCO3-, Na+ and K+, with different patterns of response being observed upon addition or deletion of these ions.

Animals↗
PubMed1998

Intratubular application of sodium azide inhibits loop of Henle reabsorption and tubuloglomerular feedback response in anesthetized rats.

Sodium azide (NaN3, AZ) is a potent inhibitor and uncoupler of oxidative phosphorylation as well as a nitrovasodilator after being converted to nitric oxide (NO). We studied the effect of intratubular application of AZ on loop of Henle reabsorption and tubuloglomerular feedback (TGF) employing renal micropuncture experiments in nephrons with superficial glomeruli of anesthetized Munich-Wistar-Fromter rats. During perfusion of Henle's loop downstream from an obstructing wax block, AZ (3x10(-5) mol/l and 3x10(-4) mol/l) concentration-dependently increased early distal tubular flow rate and sodium and potassium ion concentration (V(ED), [Na+]ED, [K+]ED). In comparison, application of furosemide (10(-4) mol/l), the action of which is restricted to the water-impermeable thick ascending limb of Henle's loop (TALH) and the macula densa, similarly increased [Na+]ED and [K+]ED, but did not affect V(ED). The effect of AZ on loop of Henle reabsorption appeared to be predominantly localized upstream to the TALH since (1) AZ significantly inhibited net fluid reabsorption (the latter being completely abolished at 3x10(-4) mol/l), (2) the effect of AZ on [Na+]ED and [K+]ED could be mimicked by perfusing the Henle's loop at a flow rate that caused a comparable increase in V(ED) (reflecting a comparable load to TALH), and (3) the effects of AZ and furosemide were additive. In spite of the increase in [Na+]ED and [K+]ED, intratubular application of AZ caused a concentration-dependent inhibition of TGF response, the latter being assessed as the fall in early proximal tubular stop flow pressure during perfusion of Henle's loop at increasing flow rate. Like AZ and furosemide, the NO donor sodium nitroprusside (10(-4) mol/l) blunted the TGF response, but in contrast to furosemide or AZ, it caused a minor decrease in V(ED), without changing [Na+]ED or [K+]ED. The inhibitory effect of AZ on TGF was abolished by the NO scavenger carboxy PTIO. In summary, AZ inhibits both reabsorption in the water-permeable segment of Henle's loop and the TGF response. The effect on reabsorption may be linked to metabolic inhibition rather than NO release, whereas the blunted TGF response appears to involve conversion to NO.

Absorption↗
PubMed1981

Characteristics of feedback control of glomerular filtration rate.

Increases in the flow rate of fluid through the loop of Henle are associated with decreases in the rate at which fluid is filtered by the glomerulus in the same nephron. The anatomical basis for this negative feedback phenomenon is very likely the close relationship between the macula densa segment of the distal tubule and the vascular components of the juxtaglomerular apparatus. Convincing evidence indicating the existence of a feedback control mechanism has come largely from micropunture experiments in which flow through single Henle loops is controlled while either filtration rate by, or capillary pressure in, the glomerulus of the same nephron is measured. Aspects of the negative feedback response that have been characterized quantitatively include the magnitude of the changes in glomerular function, the rates of tubule fluid flow that elicit the changes, and the sensitivity of the response in different physiological circumstances. Some information about the sensing step in the feedback pathway in rats has come from microperfusion experiments employing changes in the composition of fluids used to perfuse the loop of Henle or changes in the electrical driving forces across the wall of the distal tubule. Taken together, results of experiments using these different approaches indicate that changes in loop of Henle flow rate may be sensed by a process that requires transport of some constituent of distal tubule fluid, possibly the chloride ion, from the distal tubule lumen into some compartment within the juxtaglomerular apparatus.

Animals↗
PubMed1979

The effects of pressure on the water permeability of the descending limb of Henle's loops of rabbits.

Descending limbs of Henle's loops from rabbits were perfused in vitro. Using techniques where the collecting pipets permitted cannulation of the tubule, we were able to maintain reasonable flow rates at lower perfusion reservoir heights than are required with a conventional "Sylgard seal" pipet. The bath was either isosmotic to the perfusate, or was made 300 mOsm hyperosmotic using urea. Net water reabsorption did not occur in tubules perfused at low pressure (average reservoir height = 26 cm H2O) even when the bath was hyperosmotic: delta Jv = -0.06 +/- 0.18 nl/min (n = 7). Observed increases in sodium concentration and osmolality of collected fluid, when the bath was made hyperosmotic, were 16 +/- 8 mM (n - 7) and 254 +/- 38 mOsm (n = 7), respectively. Presumably the large increase in osmolality of the collected fluid was due to entrance of urea. When the "Sylgard seal" collecting end was utilized higher perfusion reservoir heights had to be used to maintain flow (mean height 66 cm H2O). These tubules were highly permeable to water as reported by others for this tubule segment. In the presence of a hyperosmotic bath water extrusion resulted in a dramatic increase in the osmolality of the collected fluid (312 +/- 5 mOsm; 7 tubules) which was almost completely accounted for by an increase in sodium concentration (153 +/- 8 mmole/l; 6 tubules). The 14C urea permeability (measured lumen to bath) of descending limbs in a 300 mOsm bath was 0.64 x 10(-7) cm2 . s-1 +/- 0.23 x 10(-7) (11 tubules). When the bath was made hyperosmotic using urea or raffinose the 14C urea permeability increased significantly.

Animals↗
PubMed1994

TNF production by the medullary thick ascending limb of Henle's loop.

Medullary thick ascending limb of Henle's loop (mTALH) tubules, isolated from kidneys of male Sprague-Dawley rats, expressed the gene for tumor necrosis factor (TNF) and released this cytokine when challenged with lipopolysaccharide (LPS). The TNF produced was biologically active, as determined by cytotoxic activity present in supernatants from LPS-stimulated mTALH, using the TNF-sensitive murine fibrosarcoma cell line, WEHI 164. The amount of TNF produced, approximately 75 nM, has previously been shown to affect ion transport in the mTALH. The TNF-mediated cytotoxicity (and ion transport effects) were completely neutralized with a polyclonal anti-TNF antisera. Further, immunoprecipitation experiments demonstrated that the 17 kDa TNF monomer was formed by de novo protein synthesis. In contrast, the mTALH did not produce the related cytokine, lymphotoxin (LT). Production of TNF was confirmed by demonstrating the accumulation of a 1.6 kb TNF mRNA by Northern blot analysis; mRNA for LT was not detected. Expression of the TNF gene in the mTALH was confirmed by the polymerase chain reaction (PCR). Southern blot analysis and ethidium bromide staining of the resultant PCR products revealed the expected 276 bp sequence of TNF DNA for the mTALH. We have demonstrated that mTALH tubules stimulated with LPS express the gene for TNF, but not LT, and release biologically active TNF. TNF is an important mediator of septic shock and may contribute to changes in renal function associated with endotoxemia. Production of TNF by the mTALH may be an important autocrine regulatory mechanism for this nephron segment.

Adjuvants, Immunologic↗
PubMed1988

Cell volume regulation by the thin descending limb of Henle's loop.

Thin descending limb cells from Henle's loop (from the inner strip of the outer medulla of long loops) were studied with optical and video techniques to identify the mechanisms of ion transport and cell volume regulation. Increasing the K+ concentration in the basolateral solution from 5 to 90 mM caused the cells to swell. This K+-induced swelling was inhibited by exposure of the basolateral membrane to 9 mM Ba2+ and was abolished by removing Cl- from the perfusion solutions. Decreasing the perfusion osmolality caused an increase in cell volume followed by a return to the preexposure volume. The latter regulatory decrease in hypoosmolality was slowed by basolateral Ba2+ and the removal of HCO-3 from the solutions. Further slowing occurred when both HCO-3 and Cl- were removed. Exposure of cells to ouabain abolished volume regulation. These data suggest that the basolateral cell membrane of the thin descending limb has a Cl- -dependent K+ permeability, which is important in cell volume regulation. The cells also possess Cl- and HCO-3 transport pathways that participate in volume regulation. Finally, volume regulation is dependent upon the operation of the Na/K pump.

Animals↗
PubMed1980

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

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.

Absorption↗
PubMed1992

Cell volume regulation in rat thin ascending limb of Henle's loop.

Thin ascending limb cells of Henle's loop from Wistar rats were studied with in vitro microperfusion and video-optical techniques to investigate their ability in regulating cell volume during osmotic shock and to identify mechanisms of ion transport involved in the process. These cells showed a clear volume regulatory decrease (VRD) response in hyposmotic medium, but no volume regulatory increase in hyperosmotic medium. The presence of barium in the bath abolished VRD. Removal of K+ from bath and perfusate also inhibited the VRD response. Reintroduction of K+ in hyposmotic conditions reestablished cell volume regulation. Introduction of anthracene-9-COOH to the basolateral medium blocked cell volume regulatory response. Cl- removal from perfusate and bath solutions also inhibited VRD, probably because of a significant intracellular Cl- depletion. Exposure of cells to ethylene glycol-bis(beta-aminoethyl ether)-N,N,N'N'-tetraacetic acid in perfusate and bath solutions reduced significantly Ca2+ concentration and impaired VRD. Reintroduction of Ca2+ in hyposmotic conditions restored volume regulation. The presence of ouabain in basolateral medium also inhibited VRD. These data suggest that the following mechanisms in the basolateral membrane are involved in VRD response: K+ and Cl- conductive pathways, which might be Ca2+ dependent for activation, and an Na(+)-K(+)-adenosinetriphosphatase.

Animals↗
PubMedDate not supplied

Ion channels in the thick ascending limb of Henle's loop.

The thick ascending limb of Henle's loop (TAL) is polarized with respect to its conductances. The luminal membrane contains a K+ conductance which is made up by the synchronous operation of 60- to 80-pS K+ channels. The basolateral membrane contains a chloride conductance. This conductance corresponds most likely to a 30- to 60-pS Cl- channel present in this membrane. Our knowledge on the properties of the K+ channels of these cells has been increased rapidly by patch clamp studies: these K+ channels are inwardly rectifying. They are highly selective for K+ over Na+, Li+ and many other cations. They do not conduct Rb+, Cs+, NH+4 or other larger cations. In fact, all these three cations as well as choline, tetraethylammonium, lidocaine, verapamil, diltiazem, quinine, quinidine and Ba2+ inhibit these K+ channels. As apparent from kinetic studies the mechanisms of inhibition are different for the various blockers. The TAL K+ channels are downregulated by increasing cytosolic Ca2+ activity. Cytosolic adenosine trisphosphate (ATP) has a similar effect. This ATP inhibition is Ca2+ dependent. The affinity to ATP is augmented by increasing Ca2+. Cytosolic alkalinity increases the open probability of these channels, and cytosolic acidification has the opposite effect. This pH dependence is very marked. A change by 0.2 pH units leads to a more than twofold change in the open-channel probability. The basolateral chloride conductance reflects the properties of an outwardly rectifying 30- to 60-pS Cl- channel. This channel behaves, in many respects, like the Cl- channels of a multitude of Cl- transporting epithelia. It is characterized by two open and two closed states. It is highly selective for Cl- as compared with larger anions, and it is inhibited reversibly by Cl- channel blockers such as 5-nitro-2-(3-phenylpropylamino)-benzoate.

Animals↗
PubMed1980

Effect of vasopressin on electrical potential difference and chloride transport in mouse medullary thick ascending limb of Henle's loop.

Medullary thick ascending limbs of Henle's loop of the Swiss-Webster mouse were perfused in vitro with an isotonic perfusate and a Ringer's bathing medium. In five studies, addition of a supramaximal concentration of synthetic arginine vasopressin (AVP) to the bathing medium resulted in an increase in electrical potential difference (PD) from 5.0 +/- 1.5 mV, lumen positive, to 10.7 +/- 1.4 mV (P < 0.001). When AVP was removed, the PD returned to 2.6 +/- 0.9 mV (P < 0.001), then increased again to 6.9 +/- 1.7 mV (P < 0.01) when AVP was added a second time. A significant, but submaximal, increase in PD of 2.3 +/- 0.6 MV (P < 0.05) was observed in five medullary thick ascending limbs when AVP was added to the bathing medium at a concentration of 10 microunits/ml. This increase was approximately one-third of the response observed at a concentration of 100 microunits/ml in the same tubule. No further increment in PD was observed in five medullary thick ascending limbs when the AVP concentration was increased from 100 to 1,000 microunits/ml. In seven thick ascendcing limbs, the effect of AVP on PD was reproduced by the addition of 8-[p-chlorophenylthio]-cyclic 3',5'-adenosine monophosphate to the bathing medium at a final concentration of 0.1 mM. AVP increased unidirectional chloride flux from lumen to bath from 29.3 +/- 3.2 to 69.8 +/- 6.2 peq/cm per s (P < 0.001) in spite of an increase in the lumen positive PD from 1.6 +/- 0.5 mV to 7.0 +/- 0.6 mV (P < 0.001). Unidirectional chloride flux from bath to lumen was not affected by AVP. In another series of experiments, net chloride flux increased from 15.6 +/- 3.0 to 41.7 +/- 5.3 peq/cm per s (P < 0.05) after addition of AVP. The effect of AVP on hydraulic water permeability (Lp) was examined by adding raffinose to the bathing medium in both the presence and the absence of AVP. The calculated Lp of 16 +/- 2 nm/s per atm in the absence of AVP, although very low, was significantly different from zero (P < 0.01). However, the Lp did not increase significantly when AVP was added to the bathing medium. These results suggest that AVP has a second site of action in the kidney to increase chloride transport by the medullary thick ascending limb in addition to its well-known effect on the water permeability of the collecting tubule. The former effect would contribute to urinary concentrating ability by increasing the axial osmotic gradient in the renal medulla.

Animals↗
PubMed1998

Transducing pathways involved in the control of NaCl reabsorption in the thick ascending limb of Henle's loop.

The thick ascending limb of Henle's loop (TAL) is involved in the urinary dilution/concentration process by actively reabsorbing NaCl through a complex mechanism. Some years ago, compelling evidence was provided that cAMP stimulates NaCl reabsorption through the activation of adenylyl cyclase by several hormones other than antidiuretic hormone (ADH). Synthesis of cyclic AMP is inhibited by prostaglandin E2 (PGE2) and arachidonic acid per se, via the pertussis toxin-sensitive protein Gi activation. Cyclic GMP cascade down-regulates NaCl reabsorption, through activation of both guanylyl cyclase receptors (by ANF and urodilatin), and soluble guanylyl cyclase (by nitric oxide, NO). In TAL, NO is produced by the cytokine-inducible form of NO synthase, but not by the constitutive one. Agonists known to activate protein kinase C (PKC) in TAL elicit opposite effects on NaCl reabsorption. Five PKC isoforms belonging to the conventional, novel, and atypical enzyme subclasses have been recently defined in TAL and might differently regulate NaCl flux. Increments in intracellular calcium ([Ca2+]i) inhibit NaCl reabsorption via three pathways: (i) a possible direct effect on ion channels, (ii) a PLA2-mediated production of arachidonic acid derivatives (20-HETE), and (iii) inhibition of the ADH-induced cAMP accumulation. This last effect results from activation of phosphodiesterase (common to the agents that increase [Ca2+]i), and inhibition of adenylyl cyclase (only elicited by Ca2+c). Finally, the apical localization of some agonists effects is documented.

Absorption↗