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PubMed2006

Sulfated HNK-1 epitope in developing and mature kidney: a new marker for thin ascending loop of Henle and tubular injury in acute tubular necrosis.

The HNK-1 carbohydrate epitope is a 3-sulfo-glucuronyl residue attached to lactosamine structures on glycoproteins, proteoglycans, or glycolipids mostly expressed in the nervous system. Here, using monoclonal antibodies against the sulfated HNK-1 carbohydrate epitope, we first examined its distribution in developing and adult kidneys, then its expression in kidneys with tubular necrosis and renal neoplasms. This HNK-1 epitope was expressed in the human, rabbit, and rat, but not mouse kidney. It was detected within a subset of epithelial cells in the renal vesicle and in comma- and S-shaped bodies during early stages of nephrogenesis. In ureteral bud derivatives, the epitope was present transiently in the area where the collecting duct fused with the nephron. In the adult kidney, expression of the HNK-1 epitope became mainly restricted to the thin ascending loop of Henle where this epitope was carried by heparan- and chondro-proteoglycan. In pathological conditions, HNK-1 epitope expression increased dramatically in proximal epithelial tubule cells in kidneys with acute tubular necrosis. In tumors, the HNK-1 epitope was expressed in the epithelial component of nephroblastomas and in a subgroup of papillary renal cell carcinomas. These data suggest that molecules carrying the sulfated HNK-1 carbohydrate epitope may play an important role in critical stages of renal development and in the physiology of thin ascending loop of Henle.

Animals↗
PubMed2002

Production of superoxide through NADH oxidase in thick ascending limb of Henle's loop in rat kidney.

We recently reported that NADH oxidase is one of the major enzymes responsible for superoxide (O(2)(-)*) production in the rat kidney. However, the functional significance of NADH oxidase-mediated O. production and the mechanisms regulating this enzyme activity are poorly understood. Using fluorescence microscopic imaging analysis, the present study demonstrated that thick ascending limbs of Henle's loop (TALHs) exhibited red fluorescence when incubated with dihydroethidium (DHE), suggesting that O(2)(-)* is produced in this tubular segment. Compared with other nephron segments, TALHs from both renal cortex and medulla showed the highest fluorescence intensity. By incubating cortical TALHs (cTALHs) with the substrates of NADH oxidase, xanthine oxidase, nitric oxide synthase, arachidonic acid-metabolizing enzymes, and intramitochondrial oxidases, NADH oxidase was found to be one of the most important enzymes for O(2)(-)* production in this tubular segment. The NADH oxidase inhibitor diphenyleneiodonium (DPI; 100 microM) completely blocked NADH-induced O(2)(-)* production in cTALHs. Exposure of cTALHs to low PO(2) (5-10 Torr) significantly increased O(2)(-)* production regardless of the absence or presence of NADH. Furthermore, angiotensin II (100 nM) increased NADH oxidase activity by 32%, which was completely blocked by DPI. These results suggest that NADH oxidase is a major enzyme responsible for O(2)(-)* production in the TALHs and that the production of O(2)(-)* via NADH oxidase may be regulated by renal tissue oxygenation and circulating hormones.

Angiotensin II↗
PubMed1991

Enhanced chloride reabsorption in the loop of Henle in Dahl salt-sensitive rats.

This study examines the nephron segments contributing to the blunted pressure-natriuretic response in Dahl salt-sensitive rats. Urine and late proximal and early distal tubular fluid samples were collected from 16-20-week-old, inbred Dahl salt-sensitive (DS/Jr) and salt-resistant (DR/Jr) rats, and Dahl salt-sensitive (DS) and salt-resistant (DR) rats from the Brookhaven colony, that were maintained from birth on a low (0.3%) sodium chloride diet. Urine flow and sodium and chloride excretions were 65% less in the DS/Jr than in the DR/Jr rats when their kidneys were perfused at an equal renal perfusion pressure of approximately 150 mm Hg. The percentages of the filtered load of water and chloride remaining at the end of the proximal tubule were significantly greater in DS/Jr rats than in DR/Jr rats; however, the percentages of the filtered load of water and chloride reaching the early distal tubule were significantly less, by 29% and 77%, respectively. Fractional reabsorption of water and chloride in the loop of Henle of DS/Jr rats was twice that observed in DR/Jr rats. Similar results were obtained in DS and DR rats of the Brookhaven strain. Urine flow and sodium and chloride excretions were 60% lower in DS than in DR rats at a renal perfusion pressure of 135 mm Hg. Proximal tubular reabsorption of water and chloride was similar in DS and DR rats; however, the percentages of the filtered load of water and chloride reabsorbed in the loop of Henle were greater in DS than in DR rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed2003

ETA receptor-mediated Ca2+ signaling in thin descending limbs of Henle's loop: impairment in genetic hypertension.

BACKGROUND: Endothelins (ET) have diuretic and natriuretic actions via ETB receptors that are found in most renal tubular segments, although the thin limbs have not been studied. Data also suggest that dysfunction of the renal ET system may be important in the pathogenesis of hypertension. The present study was aimed at determining the presence and nature of ET receptors in the thin limbs of Henle's loop and their ability to activate a Ca2+-dependent signaling pathway, as well as whether ET-induced Ca2+ signals are altered in hypertension. METHODS: Reverse transcription-polymerase chain reaction (RT-PCR) and Fura 2 fluoreselected strains of Lyon rats with low-normal (LL), normal (LN), and high (LH) blood pressure. RESULTS: In SD rats, ET induced Ca2+ signals in DTL of long-looped nephrons, but not in DTL of short loops, or in ascending thin limbs. Ca2+ increases were abolished by BQ123, an antagonist of the ETA receptor, but not by BQ788, an antagonist of the ETB subtype. Endothelin-3 and sarafotoxin 6c, two ETB receptor agonists, were both inactive. RT-PCR showed the presence of both ETA and ETB receptor mRNA. Ca2+ signals measured scence measurements of [Ca2+]i were made to characterize ET receptors in descending thin limbs (DTL) of Sprague-Dawley rats, spontaneously hypertensive (SH) rats, and control Wistar-Kyoto (WKY) rats, and the three in DTL of WKY LL and LN rats were similar to those in Sprague-Dawley rats, but were significantly diminished (LH) or abolished (SH) in hypertensive rats. CONCLUSION: A functional ETA receptor activating a Ca2+-dependent pathway is expressed in DTL. This ETA-induced calcium signaling is impaired in two strains of genetically hypertensive rats.

Animals↗
PubMed1996

Osmotic regulation of sorbitol in the thick ascending limb of Henle's loop.

Organic osmolytes, such as sorbitol, inositol, glycerophosphorylcholine, and betaine, play an important role in the osmoregulation of inner medullary cells of the kidney. The cells of the outer medulla are also exposed to elevated NaCl and urea concentrations during antidiuresis. Therefore, we investigated the mechanisms involved in the regulation of outer medullary organic osmolytes, especially cell sorbitol content of immortalized epithelial cells of the thick ascending limb of Henle's loop (TALH). In the cultured cell model, a 600 mosmol/l medium (osmolarity adjusted by addition of 150 mM NaCl or 300 mM sucrose) increased the intracellular sorbitol content significantly compared with a 300 mosmol/l medium. The accumulation of sorbitol appeared to be due to an increase of aldose reductase activity, which catalyzed sorbitol synthesis. Sorbitol degradation by sorbitol dehydrogenase was not detectable under our experimental conditions. After a sudden decrease of the extracellular osmolarity, the sorbitol permeability of the cellular membrane increased sevenfold within 10 min compared with isosmolar conditions. These results indicate that sorbitol, like inositol, plays an important role in the osmoregulation of TALH cells. Although the short-term regulation involves rapid changes in sorbitol membrane permeability, the longterm adaptation to low osmolarities is regulated by intracellular sorbitol synthesis.

Aldehyde Reductase↗
PubMed1992

Confocal microscopic and other observations on the distal end of the thick limb of the human loop of Henle.

Various antibodies and lectins were used in a histological study of the human renal tubule, particularly of the distal end of the thick limb of the loop of Henle. The thick limb, identified by antibody to Tamm-Horsfall protein, ended abruptly, either at the macula densa or at a variable distance after it. At this point there was an abrupt change in cell size. Confocal microscopy and other techniques showed that this point marked an abrupt beginning of tubular staining by the cytokeratin antibody PKK2 and the lectin UEA 1, with an abrupt end of staining by the lectin DBA. Distal from this point, there were gradual changes in staining of the tubule by various reagents including other antibodies to cytokeratins. These structural findings suggest that there is a fundamental change in the tubule at the end of the thick limb. The abrupt end to the thick limb in man resembles that seen in the rat and the rabbit.

Biomarkers↗
PubMed1982

Ammonium handling by superficial and juxtamedullary nephrons in the rat. Evidence for an ammonia shunt between the loop of Henle and the collecting duct.

Papillary and surface micropuncture was used to assess the effects of a chronic metabolic acidosis on the renal tubular handling of ammonium by surface nephrons, juxtamedullary nephrons, and the terminal segment of collecting duct. Rats chronically fed ammonium chloride had an expected decline in arterial pH and bicarbonate concentration associated with a doubling in the amount of ammonium excreted and a decline in urine pH. The glomerular filtration rate and absolute delivery of water and sodium to micropuncture sites of surface and deep nephrons was not measurably altered. Ammonium delivery to the end of the proximal tubule increased from 853+/-102% to 1,197+/-142% (SE) of the filtered load of ammonium after the induction of metabolic acidosis. This increase was due to a rise in tubular fluid ammonium content from 2.31+/-0.23 to 4.06+/-0.28 mM/liter. After the induction of acidosis, absolute and fractional delivery of ammonium ion to the end of the distal tubule was less than to the end of the accessible portion of the proximal tubule. These findings indicate that ammonium is lost in the intervening segment.Ammonium handling by deep nephrons was profoundly affected by acid loading. Absolute delivery to the bend of the loop of Henle increased twofold while fractional delivery rose from 1,222+/-108% to 1,780+/-132% of the filtered ammonium. This was due to a marked increase in ammonia entry. During acidosis, ammonium delivery to the terminal segment of the collecting duct was doubled (709+/-137% in controls vs. 1,415+/-150% in acidosis, P < 0.005) but did not change between proximal and tip collecting duct sites. In both groups of animals delivery of ammonium to the terminal segment of the collecting duct was greater than to end distal tubular micropuncture sites suggesting that ammonia entry occurred between these two sites. The differences in delivery was greater after the induction of a metabolic acidosis (887+/-140% vs. 384+/-144%, P < 0.05). Thus, the present study indicates that deep nephrons contribute to the adaptive increase in ammonium excretion seen during the induction of metabolic acidosis. The data also suggest that ammonia leaves the nephrons at a site(s) along the loop of Henle to enter the collecting duct and that the induction of a metabolic acidosis enhances this reentry.

Acidosis, Renal Tubular↗
PubMed1982

Membrane transport in the proximal tubule and thick ascending limb of Henle's loop: mechanisms and their alterations.

Over the past few years, our knowledge on renal tubular transport mechanisms has increased considerably. Due to new technical developments, it is now possible to understand in part transepithelial transport and its pathological and pharmacological alterations at the level of the cell membranes. Different membrane transport mechanisms are discussed in this article, whereby sodium coupled solute transport in the proximal tubule and sodium chloride transport in the thick ascending limb of Henle's loop are taken as examples. It is indicated that an altered function of the kidney can often be equated with an alteration of the membrane transport.

Animals↗
PubMed1987

Differentiation in vitro of primary cultures and transfected cell lines of epithelial cells derived from the thick ascending limb of Henle's loop.

The use of primary cell cultures derived from defined locations of the kidney has enabled the study of certain kidney cell type-specific characteristics under defined environmental conditions. The use of primary cell cultures, however, has a number of inherent disadvantages, many of which may be overcome by the use of differentiated cell lines of defined origin. In this paper I describe in detail an approach to: (a) the isolation and culture of primary cultures derived from the thick ascending limb of Henle's loop (TALH), and (b) the production of differentiated cell lines by the transfection of these primary cell cultures with early region SV40 virus genes. The characteristics of these cultures and other TALH-derived cell lines are described.

Animals↗
PubMed2006

Influence of body temperature on indinavir crystallization under loop of Henle conditions.

OBJECTIVES: Indinavir is a protease inhibitor used in the therapy of HIV-1+ patients. It causes indinavir stone formation. It has been shown to precipitate in the loop of Henle (LH) at plasma concentrations (conc[P]) of approximately 8 mg/L. Those experiments were performed at room temperature. Given the influence of temperature on crystallization in general, and solubility of indinavir in particular, we repeated the experiments under physiological (body) temperature conditions. METHODS: Test solutions contained indinavir concentrations of 100-750 mg/L at ionic strengths varying from 0 to 800 mM simulating conditions in the proximal tubule and the LH. Solutions were titrated with base (NaOH) to find the pH value where nucleation is initiated. Experiments were conducted at room temperature (20 degrees C) and repeated under constantly monitored (body) temperature (37 degrees C). RESULTS: Experiments at 20 degrees C confirmed our previous results. At 37 degrees C, the relationship between pH and indinavir concentration remained inversely proportional. Again, the LH was confirmed as the most likely localization of crystallization. However, at 37 degrees C precipitation occurred at a lower urinary concentration (100 versus 125 mg/L) and within a lower pH range (6.67-7.26 versus 7.23-7.44). This lower urinary concentration corresponds to a lower conc[P] [critical value (CV)] of 6.41 mg/L, as compared with 8.01 mg/L at 20 degrees C. CONCLUSIONS: The CV is even lower at 37 degrees C than previously assumed. Plasma peak concentration above the CV of 6.4 mg/L will induce crystallization in the LH and should be avoided.

Anti-HIV Agents↗
PubMed1997

Functional and structural changes in the thick ascending limb of Henle's loop in rats with liver cirrhosis.

Five weeks after common bile duct ligation (CBL), Wistar rats had histologically verified liver cirrhosis with sodium retention but without ascites. Plasma concentrations of vasopressin and aldosterone were normal. Glomerular filtration rate was unchanged, although renal plasma flow was increased. A test dose of furosemide (7.5 mg/kg body wt iv) produced significantly greater diuretic (+59%) and natriuretic (+66%) responses in Wistar CBL rats than in sham-operated controls. Stereological examination of kidneys demonstrated a 47% increase in the volume of the inner stripe of the outer medulla, with a 55% increase in the volume of thick ascending limb of Henle's loop (TALH) epithelium in cirrhotic Wistar rats relative to controls. CBL produced a similar degree of liver cirrhosis in vasopressin-deficient Brattleboro rats. However, both functional and structural renal changes observed in cirrhotic Wistar rats were absent in vasopressin-deficient cirrhotic Brattleboro rats. These results suggest a permissive action of vasopressin for the adaptive changes in TALH in rats with experimental liver cirrhosis. Our results are consistent with the hypothesis that increased sodium chloride reabsorption in the TALH may contribute to the early sodium retention that precedes ascites formation in rats with secondary biliary liver cirrhosis.

Animals↗
PubMed1979

Loop of Henle bicarbonate accumulation in vivo in the rat.

We have carried out perfusion studies on hydropenic and bicarbonate-loaded rats to provide direct in vivo observations on bicarbonate accumulation in the short loops of Henle. Analysis of early distal tubular fluid was made during bicarbonate-free saline perfusion from the end proximal to the early distal site, documenting accumulation of "new" bicarbonate. During perfusion in hydropenic rats, steady-state bicarbonate concentrations were suggested by early distal values of approximately equal to mM, which were independent of perfusion rate and virtually indistinguishable from bicarbonate concentration measured during free flow when filtered bicarbonate was allowed to enter the loop. Thus, loop bicarconate accumulation was apparently sufficient to allow new bicarbonate to enter at a rate comparable to that delivered to the early distal site during free flow, recognizing of course that free-flow delivery rates are the result of complex components of filtration and bidirectional fluxes. In bicarbonate-loaded rats, however, bicarbonate accumulation rates although higher than in hydropenia, were much lower than free-flow delivery rates. Furthermore, early distal bicarbonate concentrations during bicarbonate loading fell as perfusion rate increased, presumably because of a limitation to increasing ionic bicarbonate entry.

Animals↗
PubMed2006

Restricted localization of claudin-16 at the tight junction in the thick ascending limb of Henle's loop together with claudins 3, 4, and 10 in bovine nephrons.

Claudin-16 is one of the tight junction protein claudins and has been shown to contribute to reabsorption of divalent cations in the human kidney. In cattle, total deficiency of claudin-16 causes severe renal tubular dysplasia without aberrant metabolic changes of divalent cations, suggesting that bovine claudin-16 has some roles in renal tubule formation and paracellular transport that are somewhat different from those expected from the pathology of human disease. As the first step to clarify these roles, we examined the expression and distribution of claudin-16 and several other major claudin subtypes, claudins 1-4 and 10, in bovine renal tubular segments by immunofluorescence microscopy. Claudin-16 was exclusively distributed to the tight junction in the tubular segment positive for Tamm-Horsfall glycoprotein, the thick ascending limb (TAL) of Henle's loop, and was found colocalized with claudins 3, 4, and 10. This study also demonstrates that bovine kidneys possess segment-specific expression patterns for claudins 2-4 and 10 that are different from those reported for mice. Particularly, distribution of claudin-4 in the TAL and distal convoluted tubules was characteristic of bovine nephrons as were differences in the expression patterns of claudins 2 and 3. These findings demonstrate that the total lack of claudin-16 in the TAL segment is the sole cause of renal tubular dysplasia in cattle and suggest that the tight junctions in distinct tubular segments including the TAL have barrier functions in paracellular permeability that are different among animal species.

Amino Acid Sequence↗
PubMed1980

Volume reabsorption by the loop of Henle: a micropuncture study.

The observed extension of glomerulo-tubular beyond the proximal tube is thought to be due either to flow dependent reabsorption by non-accessible proximal segments and pars recta, or to osmotic volume flow out of the descending limb of the loop of Henle.

Animals↗
PubMed2002

Tetraethylammonium block of water flux in Aquaporin-1 channels expressed in kidney thin limbs of Henle's loop and a kidney-derived cell line.

BACKGROUND: Aquaporin-1 (AQP1) channels are constitutively active water channels that allow rapid transmembrane osmotic water flux, and also serve as cyclic-GMP-gated ion channels. Tetraethylammonium chloride (TEA; 0.05 to 10 mM) was shown previously to inhibit the osmotic water permeability of human AQP1 channels expressed in Xenopus oocytes. The purpose of the present study was to determine if TEA blocks osmotic water flux of native AQP1 channels in kidney, and recombinant AQP1 channels expressed in a kidney derived MDCK cell line. We also demonstrate that TEA does not inhibit the cGMP-dependent ionic conductance of AQP1 expressed in oocytes, supporting the idea that water and ion fluxes involve pharmacologically distinct pathways in the AQP1 tetrameric complex. RESULTS: TEA blocked water permeability of AQP1 channels in kidney and kidney-derived cells, demonstrating this effect is not limited to the oocyte expression system. Equivalent inhibition is seen in MDCK cells with viral-mediated AQP1 expression, and in rat renal descending thin limbs of Henle's loops which abundantly express native AQP1, but not in ascending thin limbs which do not express AQP1. External TEA (10 mM) does not block the cGMP-dependent AQP1 ionic conductance, measured by two-electrode voltage clamp after pre-incubation of oocytes in 8Br-cGMP (10-50 mM) or during application of the nitric oxide donor, sodium nitroprusside (2-4 mM). CONCLUSIONS: TEA selectively inhibits osmotic water permeability through native and heterologously expressed AQP1 channels. The pathways for water and ions in AQP1 differ in pharmacological sensitivity to TEA, and are consistent with the idea of independent solute pathways within the channel structure. The results confirm the usefulness of TEA as a pharmacological tool for the analysis of AQP1 function.

Animals↗
PubMed1994

Two isoforms of a chloride channel predominantly expressed in thick ascending limb of Henle's loop and collecting ducts of rat kidney.

Complementary DNAs encoding rat kidney chloride channels (ClC-K2L and ClC-K2S) were isolated by a polymerase chain reaction cloning strategy. Degenerate primers were designed based on the significant amino acid identity of the previously cloned chloride channels (ClC-0, -1, -2, and -K1). The 687-amino acid protein encoded by ClC-K2L is about 80% identical to rat ClC-K1 and about 40% identical to ClC-0, -1, and -2. ClC-K2S encodes a 632-amino acid protein in which 55 amino acids containing the putative second membrane-spanning domain of ClC-K2L are deleted. Chloride currents induced by both clones were very similar in terms of inhibitor sensitivity and anion selectivity (Br- > I- > Cl- >> cyclamate-). Northern blot with total ClC-K2L as a probe under high stringency revealed its message predominantly in kidney, especially in the outer and inner medulla. Reverse transcription polymerase chain reaction technique using microdissected nephron segments revealed that the main site of expression of both clones in kidney was the thick ascending limb of Henle's loop and collecting ducts, where the existence of a variety of chloride channels and their importance for maintaining body fluid homeostasis have been demonstrated. These results suggest that ClC-K2L and -K2S are chloride channels in the thick ascending limb and collecting ducts and may be important routes for transcellular chloride transport like ClC-K1.

Amino Acid Sequence↗
PubMed2006

Intrarenal octreotide treatment prevents sodium retention in liver cirrhotic rats: evidence for direct effects within the thick ascending limb of Henle's loop.

We have previously shown that systemic treatment with the somatostatin analog octreotide has marked beneficial effects on renal function in rats with liver cirrhosis induced by common bile duct ligation (CBL; Jonassen TEN, Christensen S, Sørensen AM, Marcussen N, Flyvbjerg A, Andreasen F, and Petersen JS. Hepatology 29: 1387-1395, 1999). In the present study, we tested the hypothesis that octreotide has a direct effect on renal tubular function. Rats (CBL or Sham-CBL) were intrarenally treated with low-dose octreotide in a long-acting release formulation, which had no systemic actions (100 microg/kg body wt as a single dose). Rats receiving low-dose octreotide (sc) were used as controls. The rats were chronically instrumented, and renal function was examined 4 wk after CBL or Sham-CBL. Intrarenal octreotide administration (IROA) prevented sodium retention in CBL rats without changes in renal plasma flow, glomerular filtration rate, or circulating levels of aldosterone and vasopressin. Renal clearance studies revealed that IROA normalized the increased natriuretic efficacy of furosemide found in CBL rats. Furthermore, IROA protected against the development of hypertrophy of the inner stripe of the outer medulla and thereby the increased the volume of thick ascending limb of Henle's loop (TAL) epithelium found in CBL rats. Finally, Western blot analyses of outer medullary homogenates showed increased abundance of the furosemide-sensitive Na-K-2Cl (NKCC2) cotransporter. IROA did not affect the abundance of NCKK2 within the outer medulla. Together with the histological findings, these results indicate that IROA reduces the total number of NKCC2 within the outer medulla. In conclusion, the results indicate a direct intrarenal effect of octreotide on TAL function and morphology in cirrhotic rats.

Animals↗