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PubMed1991

An NMR spectroscopic characterization of a new epithelial cell line, TALH-SVE, with properties of the renal medullary thick ascending limb of Henle's loop.

NMR spectroscopy has been used to characterize a new renal cell line, TALH-SVE.1, which is derived from the medullary thick ascending limb of Henle's loop. From the 31P-NMR spectrum of a suspension of TALH-SVE cells using the chemical shift of the intracellular inorganic phosphate a value of 7.24 +/- 0.04 for the steady-state intracellular pH (pHi) was determined at pHo = 7.40. In addition, the 31P-NMR spectrum indicated rather high levels of UDPG, a finding confirmed by 1H-NMR spectra of perchloric acid extracts. The 1H-NMR data also demonstrate the presence of 'organic osmolytes' such as inositol, sorbitol, choline and glycerophosphoryl choline (GPC). 13C-NMR spectra of perchloric acid extracts of TALH-SVE cells incubated with [2-13C]- and [3-13 C]alanine were used to determine the relative influx in the Krebs cycle via pyruvate carboxylase (PCB) versus the influx via pyruvate dehydrogenase (PDH). The ratio was 0.41, while about 52% of all acetyl-CoA entering the Krebs cycle was unlabeled. 13C-NMR experiments also indicated that TALH-SVE cells lack gluconeogenic activity. The NMR study presented indicates that TALH-SVE cells possess metabolic pathways similar to those of the parental cells.

Alanine↗
PubMed1993

Structural-functional correlation in chinchilla long loop of Henle thin limbs: a novel papillary subsegment.

The ultrastructural characteristics of thin limb subsegments from chinchilla long loops of Henle were studied in perfusion-fixed kidneys and in isolated perfused tubules. In sections from the perfusion-fixed kidneys, we noted types I, II, III, and IV thin limb epithelia similar to those previously identified in other rodent species. Sections from the deepest 20% of the papillary tip, however, revealed only a single thin limb epithelial type, which had a combination of structural characteristics distinct from previously identified thin limb subtypes. This "papillary type" epithelium had relatively tall cells and a complex cellular organization with extensive interdigitation, numerous shallow tight junctions, and microvilli. In single-tubule studies, thin limb segments dissected from different levels of the outer and inner medulla were perfused in vitro for osmotic water permeability (Pf) measurements and were fixed for ultrastructural examination. Long-loop thin descending limbs (LDL) dissected from the outer medulla (Pf, 2,637 +/- 336 micron/s) had type II epithelium. LDL dissected from the middle of the inner medulla (Pf, 1,570 +/- 76 microns/s) had a type III epithelium. LDL segments dissected from the deepest 20% of the inner medulla had a low but nonzero Pf (68 +/- 9 micron/s) and had the same novel papillary type epithelium seen in sections from fixed kidneys. Thin ascending limbs dissected from inner 50% of the inner medulla had essentially zero Pf (8 +/- 4 micron/s) and had a type IV epithelium. Immunohistochemical localization of CHIP28 water channel protein confirmed the presence of CHIP28 in thin descending limbs throughout the outer 75% of the inner medulla, whereas labeling was essentially absent in the deep inner medulla where the low-PfLDL (novel papillary type epithelium) is located.

Animals↗
PubMed1993

Hormonal stimulation of Ca2+ and Mg2+ transport in the cortical thick ascending limb of Henle's loop of the mouse: evidence for a change in the paracellular pathway permeability.

Recent studies from our laboratory have shown that in the cortical thick ascending limb of Henle's loop of the mouse (cTAL) Ca2+ and Mg2+ are reabsorbed passively, via the paracellular shunt pathway. In the present study, cellular mechanisms responsible for the hormone-stimulated Ca2+ and Mg2+ transport were investigated. Transepithelial voltages (PDte) and transepithelial ion net fluxes (JNa, JCl, JK, JCa, JMg) were measured in isolated perfused mouse cTAL segments. Whether parathyroid hormone (PTH) is able to stimulate Ca2+ and Mg2+ reabsorption when active NaCl reabsorption and thus PDte, is abolished by luminal furosemide was first tested. With symmetrical lumen and bath Ringer's solutions, no Ca2+ and Mg2+ net transport was detectable, either in the absence or in the presence of PTH. In the presence of luminal furosemide and a chemically imposed lumen-to-bath directed NaCl gradient, which generates a lumen-negative PDte, PTH slightly but significantly increased Ca2+ and Mg2+ net secretion. In the presence of luminal furosemide and a chemically imposed bath-to-lumen-directed NaCl gradient, which generates a lumen-positive PDte, PTH slightly but significantly increased Ca2+ and Mg2+ net reabsorption. In view of the observed small effect of PTH on passive Ca2+ and Mg2+ movement, a possible interference of furosemide with the hormonal response was considered. To investigate this possibility, Ca2+ and Mg2+ transport was first stimulated with PTH in tubules under control conditions. Then active NaCl reabsorption was abolished by furosemide and the effect of PTH on JCa and JMg measured. In the absence of PDte and under symmetrical conditions, no Ca2+ and Mg2+ transport was detectable, either in the presence or absence of PTH. In the presence of a bath-to-lumen-directed NaCl gradient, Ca2+ and Mg2+ reabsorption was significantly higher in the presence than in the absence of PTH. Finally, when active NaCl transport was not inhibited by furosemide, but reduced by a bath-to-lumen-directed NaCl gradient, PTH strongly increased JCa and JMg, whereas only a small increase in PDte was noted. In conclusion, these data suggest that PTH exerts a dual action on Ca2+ and Mg2+ transport in the mouse cTAL by increasing the transepithelial driving force for Ca2+ and Mg2+ reabsorption through hormone-mediated PDte alterations and by modifying the passive permeability for Ca2+ and Mg2+ of the epithelium, very probably at the level of the paracellular shunt pathway.

Animals↗
PubMed1989

Piretanide-dextran and piretanide-polyethylene glycol interact with high affinity with the Na+ 2 Cl- K+ cotransporter in the thick ascending limb of the loop of Henle.

Piretanide blocks the Na+ 2Cl- K+ cotransporter protein in the thick ascending limb (TAL) of the loop of Henle reversibly. When tested from the luminal side in isolated perfused cTAL segments it leads to a half maximal inhibition (IC50) of the equivalent short circuit current (Isc) at a concentration of 10(-6) mol/l. From the basolateral side it has no effect on Isc up to 10(-4) mol/l. The present study was designed to search for high affinity blockers of the Na+ 2Cl- K+ cotransporter with large molecular weight in an attempt to use these macromolecules for antibody-labelling or affinity separation of this transport-protein. Amino-ethyl-dextran or amino-ethyl-polyethylene glycol (M.W. 5kd) were coupled to isothiocyanato-piretanide (ISO-PIR) at room temperature in DMSO. The resulting compounds dextran-sulfonylurea-piretanide (PIR-DEX) and polyethylene glycol-sulfonylurea-piretanide (PIR-PEG) (M.W. 5.38kd) were purified and tested in isolated perfused cTAL segments. IC50 values for ISO-PIR, PIR-DEX and PIR-PEG were estimated from dose response curves after their addition to the lumen or bath perfusate, respectively. ISO-PIR, PIR-DEX and PIR-PEG acted from the lumen side at 3.10(-6), 6.10(-6) and 2.10(-6) mol/l. The inhibitory effect was easily reversible. From the basolateral side no effect for any compound was seen at up to 10(-4) mol/l. In clearance experiments PIR-DEX was given to female Wistar rats as an i.v. bolus (25 mumol/kg) and the diuretic urine was collected. After dialysis (exclusion limit 2.5kd) the dialysed urine and the dialysate were tested in isolated perfused cTAL segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

cAMP increases the basolateral Cl- -conductance in the isolated perfused medullary thick ascending limb of Henle's loop of the mouse.

The effect of cAMP on transepithelial and transmembrane potential differences and resistances was examined in isolated in vitro perfused mouse medullary thick ascending limbs of Henle's loop (mTAL). The effects of furosemide and barium were tested. Stimulation of NaCl transport by ADH 10(-9) + dbcAMP 4 X 10(-4) + forskolin 10(-6) mol X l-1 (paired experiments) resulted in: a) an increase in transepithelial potential difference, referenced to the grounded bath, from +6.7 +/- 0.3 mV to +12.0 +/- 0.4 mV (n = 47); b) a decrease in transepithelial resistance from 25 +/- 1 omega cm2 to 20 +/- 1 omega cm2 (n = 47); c) a depolarization of the basolateral membrane by 12 mV and of the apical membrane by 7 mV (n = 36); d) a decrease in the fractional resistance of the basolateral membrane from 0.27 +/- 0.05 to 0.15 +/- 0.06 (n = 12). Furosemide (10(-4) mol X l-1) abolished the active transepithelial transport potential and hyperpolarized the basolateral membrane potential to values which were similar in both control and cAMP treated mTAL segments. Barium increased the transepithelial resistance and depolarized PDb1 to similar values in both functional states. An increase in the fractional conductance of the basolateral membrane was also seen, if, prior to the cAMP treatment, the luminal Na+2Cl-K+ cotransport was inhibited by furosemide. Thus, we propose that stimulation of active NaCl reabsorption in the mTAL segment of the mouse by ADH, mediated via cAMP, increases primarily the basolateral chloride conductance.

Animals↗
PubMed1989

The vulnerability of the thin descending limbs of Henle's loop in the isolated perfused rat kidney.

In the isolated rat kidney perfused without erythrocytes, the medullary thick ascending limb shows extensive injury. Damage to the thin limbs of Henle's loop has been mentioned only briefly. Thin limbs were examined in the isolated perfused kidney under a variety of conditions that alter oxygenation and active transport in the medulla and are known to affect injury to the medullary thick ascending limb. The thin descending limbs of short loops were preserved in all experimental groups, but those of the long loop showed necrosis that was restricted to the proximal portion, where the epithelium is more complex. In oxygenated kidneys, necrosis involved 41% +/- 5% (mean +/- SE) of the medullary thick ascending limbs and 10% +/- 3% of the proximal portion of long loops of thin descending limbs. Under hypoxic conditions, necrosis involved 90% +/- 3% of the medullary thick ascending limbs and 70% +/- 5% of the proximal portion of long loops of thin descending limbs (P less than 0.0001 compared with oxygenated kidneys). Ouabain and absence of filtration completely prevented necrosis of both nephron segments. Thus, the proximal portions of long loops of thin descending limbs, in resemblance to medullary thick ascending limbs, are especially susceptible to transport-dependent hypoxic injury.

Animals↗
PubMed1986

Modulation by verapamil of hormonal action on the Henle's loop of mice.

In order to know the role of cytosolic calcium in the modulation of the hormone action on sodium chloride transport across the thick ascending limbs of Henle's loop, we examined whether verapamil, a blocker of cellular calcium entry, can modulate the effects of arginine vasopressin (AVP) or glucagon in stimulating transepithelial voltage (Vt) and cyclic AMP generation in the mouse medullary thick ascending limb (MAL). The pretreatment of the renal tubule with 5 X 10(-5)M verapamil reduced the Vt stimulated with 200 microU/mliter AVP from 1.7 +/- 0.3 mV to 0.4 +/- 0.4 mV (N = 7, P less than 0.05). The changes in Vt were well correlated with those of unidirectional Cl flux from the lumen to the bath. However, verapamil did not influence the Vt stimulated with 10(-3) M dibutyryl cyclic AMP. The pretreatment of the MAL with 10(-5) M verapamil also inhibited the cyclic AMP generation in the MAL from 72.1 +/- 17.9 to 50.6 +/- 13.6 fmoles/mm/7 min (N = 7, P less than 0.05) as well as in the medullary collecting tubule from 147.6 +/- 46.6 to 121.2 +/- 41.6 fmoles/mm/7 min (N = 4, P less than 0.05). The effect of verapamil in inhibiting the AVP-stimulated cAMP was dose-dependent: the cAMP generation was inhibited by 28.9 +/- 6.8 and 61.1 +/- 9.3% with 10(-5) M and 10(-4) M verapamil, respectively. When verapamil was added to the medium simultaneously with AVP, the generation of cyclic AMP was unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Evidence supporting a role for KCl cotransporter in the thick ascending limb of Henle's loop.

BACKGROUND: A basolateral Ba(2+)-sensitive KCl cotransporter has previously been proposed as participating in basolateral K+ recycling and transepithelial NaCl reabsorption in the thick ascending limb of Henle's loop (TAL). The aim of the present study was to answer the question as to whether this cotransporter plays a role in transepithelial K+ reabsorption and whether dietary Mg(2+) deficiency, known to regulate the KCl cotransporter in erythrocytes, also regulates KCl transport in the TAL. METHODS: The effects of a low-Mg(2+) diet were investigated on urinary and plasma K+ concentration in control mice and Mg(2+)-deficient mice. Transepithelial Na+, Cl- and K+ net fluxes (J(Na), J(Cl), J(K)), determined in isolated perfused TALs with electron probe analysis or cation-exchange high-performance liquid chromatography (HPLC) and electrophysiological parameters (V(te), R(te)), were measured in both animal groups. Expression of transcripts for the KCl cotransporter and its possible regulation by low-Mg(2+) were studied by RT-PCR in microdissected mouse cortical TAL (CTAL) and medullary TAL (MTAL) segments. RESULTS: In isolated perfused CTALs, basolateral Ba(2+) and amiloride induced a large K+ net secretion towards the tubular lumen, paralleled by a 50% decrease in transepithelial NaCl reabsorption. KCC1 transcripts were found in the mouse CTAL and MTAL. A low-Mg(2+) diet led to diminished urinary K+ excretion, lowered plasma K+ concentration and up-regulation of KCC1 transcripts in the TAL. For low-Mg(2+) diet, this upregulation was associated with increased transepithelial K+ reabsorption in the in vitro-perfused CTAL. CONCLUSIONS: Our study provides evidence that the KCl cotransporter, which is functionally expressed in the TAL, plays an important role in transepithelial K+ reabsorption. Direct inhibition of this transporter by Ba(2+) and its indirect inhibition by amiloride lead to a strong transepithelial K+ secretion and diminished NaCl reabsorption in the TAL. Up-regulation of KCC1 mRNA by dietary Mg(2+) restriction is associated with an increased K+ reabsorption in the in vitro perfused CTAL.

Acetonitriles↗
PubMed1983

Sodium-chloride transport in the medullary thick ascending limb of Henle's loop: evidence for a sodium-chloride cotransport system in plasma membrane vesicles.

Sodium transport mechanisms were investigated in plasma membrane vesicles prepared from the medullary thick ascending limb of Henle's loop (TALH) of rabbit kidney. The uptake of 22Na into the plasma membrane vesicles was investigated by a rapid filtration technique. Sodium uptake was greatest in the presence of chloride; it was reduced when chloride was replaced by nitrate, gluconate or sulfate. The stimulation of sodium uptake by chloride was seen in the presence of a chloride gradient directed into the vesicle and when the vesicles were equilibrated with NaCl, KCl plus valinomycin so that no chemical or electrical gradients existed across the vesicle (tracer exchange experiments). Furosemide decreased sodium uptake into the vesicles in a dose-dependent manner only in the presence of chloride, with a Ki of around 5 X 10(-6) M. Amiloride, at 2 mM, had no effect on the chloride-dependent sodium uptake. Similarly, potassium removal had no effect on the chloride-dependent sodium uptake and furosemide was an effective inhibitor of sodium uptake in a potassium-free medium. The results show the presence of a furosemide-sensitive sodium-chloride cotransport system in the plasma membranes of the medullary TALH. There is no evidence for a Na+/H+ exchange mechanism or a Na+ -K+ -Cl- cotransport system. The sodium-chloride cotransport system would effect the uphill transport of chloride against its electrochemical potential gradient at the luminal membrane of the cell.

Anions↗
PubMedDate not supplied

Transepithelial Ca2+ and Mg2+ transport in the cortical thick ascending limb of Henle's loop of the mouse is a voltage-dependent process.

The mechanisms responsible for transepithelial Ca2+ and Mg2+ in transport in the isolated perfused cortical thick ascending limb (cTAL) of Henle's loop of the mouse nephron were investigated by measuring transepithelial voltages (PDte) and transepithelial ion net fluxes (JNa, JCl, JK, JCa, JMg) by electron microprobe analysis. In the presence of furosemide (10(-4) mol.l-1, lumen) and diphenylamine-2-carboxylate (DPC, 10(-4) mol.l-1, bath), known inhibitors of NaCl reabsorption in the TAL, Ca2+ and Mg2+ reabsorption was completely inhibited. In the presence of furosemide, JCa fell from 0.75 +/- 0.07 to -0.08 +/- 0.09 pmol.min-1.mm-1 (n = 5), and JMg from 0.47 +/- 0.04 to -0.01 +/- 0.11 pmol.min-1.mm-1 (n = 5). In the presence of DPC, JCa fell from 0.57 +/- 0.08 to -0.07 +/- 0.11 pmol.min-1.mm-1 (n = 5), and JMg from 0.16 +/- 0.02 to -0.11 +/- 0.07 pmol.min-1.mm-1 (n = 5). With furosemide, inhibition of Ca2+ and Mg2+ transport was paralleled by a 93% inhibition of NaCl reabsorption, while in the presence of DPC there was a 60% reduction of NaCl reabsorption. These effects were fully reversed after removal of the inhibitors from the lumen or bath solutions. In the absence of active NaCl transport, a lumen-to-bath directed-NaCl gradient (lumen: 150 mM NaCl + furosemide, bath: 50 mM NaCl + 200 mM mannitol) generated a negative transepithelial dilution potential of -13.8 +/- 1.1 mV (n = 8) which induced a significant Ca2+ and Mg2+ secretion into the tubular lumen of -0.59 +/- 0.06 and -0.43 +/- 0.05 pmol.min-1.mm-1 (n = 8), respectively. A bath-to-lumen-directed NaCl gradient, on the other hand, (lumen: 50 mM NaCl + furosemide, bath: 150 mM NaCl) generated a positive transepithelial dilution potential of +15.9 +/- 0.6 mV (n = 7), inducing a significant Ca2+ and Mg2+ reabsorption of 0.62 +/- 0.08 and 0.38 +/- 0.07 pmol.min-1.mm-1 (n = 7), respectively. Linear regression analysis of individual Ca2+ and Mg2+ net flux data versus voltage indicated that JCa and JMg were highly correlated to PDte. In conclusion, these data indicate that transepithelial Ca2+ and Mg2+ reabsorption in the mouse cTAL is predominantly a passive process, driven by the lumen-positive PDte.

Absorption↗
PubMed1989

Stimulation of ornithine decarboxylase activity by arginine vasopressin in the rat medullary thick ascending limb of Henle's loop.

The effect of arginine vasopressin (AVP) on rat renal ornithine decarboxylase (ODC) activity was investigated by a cytochemical technique optimized for use in the medullary thick ascending limb of Henle's loop (mTAL). Stimulation of ODC activity by AVP was confined to the mTAL. Peaks in enzyme activity in cultured rat renal segments occurred after tissue had been exposed to AVP for 3 or 8 min and these times of maximal stimulation did not change with the concentration of AVP. There was a dose-dependent response in ODC activity over the AVP concentration range 0.01 10 fmol/l. The ODC response to AVP was totally blocked by specific antiserum to AVP and reduced by 70% with the specific inhibitor to ODC, difluoromethyl ornithine.

Animals↗
PubMed1985

Active chloride transport in rabbit thick ascending limb of Henle's loop and elasmobranch rectal gland: chloride fluxes in isolated plasma membranes.

To investigate directly whether a sodium-potassium-chloride cotransport system is operating in the mammalian thick ascending limb of Henle's loop (TALH) and in the elasmobranch rectal gland, plasma membrane vesicles were prepared from TALH cells isolated from rabbit kidney outer medulla and from rectal glands of Squalus acanthias, and chloride uptake was measured by a rapid filtration technique. Chloride uptake into TALH vesicles in the presence of a 25 mM Na2SO4, 25 mM K2SO4 gradient reached 70% of equilibrium at 2.5 min. In the presence of both sodium and potassium, the 15 s chloride uptake was inhibited 35% by 1 mM bumetanide. When either sodium or potassium was removed from the incubation medium, chloride uptake decreased to the level observed in the presence of 1 mM bumetanide, 0.5 mM SITS had no effect on chloride uptake by the plasma membrane vesicles. This sodium and potassium dependent, bumetanide sensitive chloride uptake was also observed under tracer exchange conditions. Chloride uptake into rectal gland plasma membrane vesicles in the presence of a 50 mM Na2SO4, 50 mM K2SO4 gradient reached 80% of equilibrium at 2.5 min. 1 mM bumetanide inhibited the 15 s uptake of chloride by 34% and removal of either sodium or potassium from the incubation medium reduced chloride uptake to the level observed in the presence of bumetanide under both gradient and tracer exchange conditions. These studies provide additional support for the hypothesis that a sodium-potassium-chloride cotransport system is operating in these epithelia.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1988

Effect of high protein intake on sodium, potassium-dependent adenosine triphosphatase activity in the thick ascending limb of Henle's loop in the rat.

1. We have previously shown that the hypertrophy of the kidney induced by a high protein diet consists of a preferential hypertrophy of the thick ascending limb (TAL) of Henle's loop. This might be related to an increase in the active salt transport by this segment. Sodium, potassium-dependent adenosine triphosphatase (Na+,K+-ATPase) activity was measured in TAL from kidneys of rats fed either a low (LP) or a high (HP) protein diet for several weeks. 2. Enzymatic activity was measured by microdensitometry, after appropriate cytochemical reaction, for an adenosine 5'-triphosphate (ATP) concentration of 0-66 mmol/l. Both activity per unit tubular length and mean activity per unit tissue volume were recorded. A calibration was designed to convert usual microdensitometry units (extinction) into conventional biochemical units (mol of product formed). 3. For non-limiting substrate concentrations, the Na+,K+-ATPase activity, expressed per unit length of tubule on the sections, was 50% higher in HP than in LP rats, an increase proportional to that of the simultaneously measured tubule diameter. When expressed per unit tubular volume, Na+,K+-ATPase activity was similar in both groups of rats. The dissociation constant for ATP was also similar in both groups. 4. Results show that a high protein diet induces an increase in Na+,K+-ATPase activity in TAL, thus enabling an enhanced NaCl transport in this segment. This increase in transport capacity is not due to an increase in the density of enzymatic units but to an increase in their number, in relation to the hypertrophy of the TAL.

Animals↗
PubMed1990

Stimulation of Na+/K(+)-ATPase activity by polyamines in the rat renal medullary cells of the thick ascending limb of Henle's loop.

Previous studies have indicated that ornithine decarboxylase (ODC) may be involved in the stimulation of Na+/K(+)-ATPase activity by arginine vasopressin (AVP) in the rat renal medullary thick ascending limb of Henle's loop. The present study was aimed at establishing the role of the polyamines, the conversion products of ODC activity, in the stimulation of Na+/K(+)-ATPase by AVP. Using cytochemical methods, we have demonstrated an increase in Na+/K(+)-ATPase activity after stimulation with putrescine, spermidine and spermine (each 1 mmol/l) for 2.5, 2 and 1.5 min respectively. The specific inhibitors of spermidine and spermine synthase, bis-cyclohexylammonium sulphate and N-alkylated-1,3-diaminopropane respectively, inhibited the stimulation of Na+/K(+)-ATPase by AVP, this inhibition being reversed by spermine. These findings suggest that polyamines are involved in the stimulus-response coupling of the hormone-mediated response.

Animals↗
PubMed1989

Effects of glucagon on H(+)-HCO3- transport in Henle's loop, distal tubule, and collecting ducts in the rat.

Paired micropuncture experiments were carried out in somatostatin-infused volume-expanded rats to examine the effects of a glucagon infusion (0.05 ng.min-1.g body wt-1) on urinary acidification and tubular handling of bicarbonate. Whole kidney and single-nephron glomerular filtration rate were not affected by glucagon. In thyroparathyroidectomized (TPTX) rats, glucagon inhibited the reabsorption of total CO2 in Henle's loop. In intact animals, however, the latter effect was not observed. In the distal tubule accessible to micropuncture, net total CO2 absorption was observed during volume expansion plus somatostatin infusion, which reversed to net total CO2 secretion during glucagon infusion in Wistar rats; thus the late distal delivery of total CO2 increased almost 80%. Marked inhibition of urinary acidification occurred in all animals as evidenced by a rise in urine pH and bicarbonate excretion. Conversely, a somatostatin infusion, which decreased the plasma glucagon concentration, stimulated net total CO2 absorption along the distal tubule and augmented final urine acidification in Wistar rats. Finally, urine-minus-blood PCO2 during alkaline diuresis was significantly reduced by glucagon infusion in bicarbonate-loaded TPTX rats. We conclude that 1) glucagon inhibits bicarbonate absorption in superficial Henle's loop in TPTX but not in intact rats, and 2) glucagon stimulates bicarbonate secretion and/or inhibits proton secretion in the distal tubule and collecting ducts, which leads to reduced urinary acidification.

Animals↗
PubMed1991

Calcium transport in the proximal convoluted tubule and loop of Henle of rats made diabetic with streptozotocin.

In-vivo microperfusion was used to localize the reabsorptive defect responsible for the hypercalciuria of diabetes mellitus and to investigate possible causative factors. Unidirectional proximal calcium absorption was not significantly different in rats made diabetic with streptozotocin compared with controls, providing evidence against the involvement of this nephron segment in the phenomenon. Calcium absorption by the loop of Henle, was however, significantly (P less than 0.01) lower in diabetic animals (32.1 +/- 1.2 vs 40.4 +/- 0.6 pmol/min). Based on our knowledge of calcium movements within the loop, it is likely that the reabsorptive defect residues within the thick ascending limb. The calcium lesion was found to be independent of acute changes in intraluminal glucose concentration and could not be corrected by acute insulin treatment. The study also provides new information on the relationship between intratubular glucose and fluid movements in the rat nephron. In diabetic rats a proximal perfusate containing 30 mmol glucose/l resulted in fluid absorption comparable with that seen in control rats perfused with 5 mmol glucose/l. However, intraluminal glucose had a stimulatory effect on fluid absorption in the loop of Henle of diabetic rats (10.7 +/- 0.5 vs 7.9 +/- 0.4 nl/min; P less than 0.01).

Absorption↗
PubMed1979

The ultrastructural localization of membrane ATPase in rat thin limbs of the loop of Henle.

The cytochemical distribution of nonspecific membrane ATPase activity in the epithelial membranes of the thin limbs of the loops of Henle of rat nephrons was studied at the ultrastructural level. Membrane ATPase activity was localized in the luminal, lateral, and (to a lesser extent) basal membranes of only the outer medullary segment of the thin descending limbs of long nephrons (Type II epithelium). The reaction product was lacking in the thin limb of short nephrons (Type I epithelium) as well as in the inner medullary descending (Type III epithelium) and ascending (Type IV epithelium) segments of the thin limbs of long nephrons. These data reinforce the concept of thin limb heterogeneity and may indicate a specialized role for the outer medullary segment of thin descending limbs of long nephrons in the concentrating mechanism.

Adenosine Triphosphatases↗
PubMed1989

Interaction between loop of Henle flow and arterial pressure as determinants of glomerular pressure.

Experiments were performed in anesthetized rats to study the relationship between loop of Henle perfusion rate, arterial pressure, and stop-flow pressure (SFP) as an index of glomerular capillary pressure. In one set of experiments we measured the SFP feedback response to changes in loop perfusion at three levels of arterial pressure. The maximum SFP response fell significantly from 13.1 +/- 1.44 to 8.14 +/- 1.72 and 3.13 +/- 0.76 mmHg when arterial pressure was reduced from 118.1 +/- 1.27 to 98.8 +/- 0.51 and 78.8 +/- 1.72 mmHg. In other experiments arterial pressure was altered while loop perfusion rate was fixed at one of three levels. Without loop perfusion SFP changed with a slope of 0.27 +/- 0.04 mmHg/mmHg in the arterial pressure range between 80 and 130 mmHg. During perfusion at the flow rate at which response is half maximum, the slope was significantly reduced to 0.12 +/- 0.04. During perfusion at 45 nl/min, it was 0.03 +/- 0.05, a value not significantly different from zero. During dopamine administration (70 micrograms/kg min) SFP was pressure-dependent even during loop perfusion at 45 nl/min. These results show that arterial pressure determines TGF responsiveness and that the TGF signal determines the range of a regulatory input that is directly dependent on arterial pressure.

Animals↗