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PubMedDate not supplied

Vitamin A excreted in the urine of canines is associated with a Tamm-Horsfall like protein.

Under physiological conditions canines transport vitamin A in blood plasma primarily as retinyl esters bound to lipoproteins and excrete substantial amounts of vitamin A as retinol and retinyl esters with urine. In the aqueous environment of urine, the hydrophobic vitamin A has to be associated with a protein. This vitamin A-protein complex was purified to homogeneity, prepared by preparative ultracentrifugation (density 1.21 g/mL), native polyacrylamide gel electrophoresis (PAGE) and size exclusion chromatography. The vitamin A-protein complex has a high molecular mass of > 5,000 kDa under native conditions. SDS PAGE under reduced conditions revealed a single band with a molecular mass of about 100 kDa for the protein moiety. Peptides obtained after limited proteolysis with trypsin from the 100 kDa protein were characterised by MALDI-TOF mass spectrometry and showed amino acid sequence homology to the human Tamm-Horsfall Protein (THP). This was further confirmed by a positive immunoreaction of the isolated protein with crossreacting human THP antibodies. The localisation of THP in dog kidneys was determined by using immunohistology. The reaction was strong along the entire thick ascending limb ofthe Henle loop and distal convoluted tubule. Our data point to the possibility that THP functions as a novel carrier for vitamin A in the urine of canines.

Amino Acid Sequence↗

PubMed1998

Osmoregulatory function of the kidney in enuretic children.

Twenty children with primary nocturnal enuresis and 20 healthy children of the same age and sex were studied. Natural urination was used for the 24-h urine collection. It was found that urine osmolality and free water reabsorption during the night did not differ statistically significantly between the enuretic children and the healthy. The increased diuresis in the enuretic children was caused by a higher excretion of the osmotically active solutes, including sodium. Use of desmopressin reduced diuresis and natriuresis to normal levels. It is suggested that the main role in the pathogenesis of the studied form of nocturnal enuresis is played by a decrease in ion reabsorption, probably in the thick ascending Henle loop, which facilitates the increase in diuresis and occurrence of nocturnal enuresis.

Adolescent↗

PubMed1993

CHIP28 water channels are localized in constitutively water-permeable segments of the nephron.

The sites of water transport along the nephron are well characterized, but the molecular basis of renal water transport remains poorly understood. CHIP28 is a 28-kD integral protein which was proposed to mediate transmembrane water movement in red cells and kidney (Preston, G. M., T. P. Carroll, W. B. Guggino, and P. Agre. 1992. Science [Wash. DC]. 256:385-387). To determine whether CHIP28 could account for renal epithelial water transport, we used specific polyclonal antibodies to quantitate and localize CHIP28 at cellular and subcellular levels in rat kidney using light and electron microscopy. CHIP28 comprised 3.8% of isolated proximal tubule brush border protein. Except for the first few cells of the S1 segment, CHIP28 was immunolocalized throughout the convoluted and straight proximal tubules where it was observed in the microvilli of the apical brush border and in basolateral membranes. Very little CHIP28 was detected in endocytic vesicles or other intracellular structures in proximal tubules. Uninterrupted, heavy immunostaining of CHIP28 was also observed over both apical and basolateral membranes of descending thin limbs, including both short and long loops of Henle. These nephron sites have constitutively high osmotic water permeabilities. CHIP28 was not detected in ascending thin limbs, thick ascending limbs, or distal tubules, which are highly impermeable to water. Moreover, CHIP28 was not detected in collecting duct epithelia, where water permeability is regulated by antidiuretic hormone. These determinations of abundance and structural organization provide evidence that the CHIP28 water channel is the predominant pathway for constitutive transepithelial water transport in the proximal tubule and descending limb of Henle's loop.

Animals↗

PubMed1969

Electron microscope studies on the surface coat of the nephron.

Attempts to make visible the carbohydrate coat at the free cell surface of glomeruli as well as the tubules of rabbit kidney were undertaken. The ruthenium red procedure was performed, according to Luft, at various pH values. Moreover, the colloidal iron and the colloidal thorium methods were used. Neuraminidase digestion was also performed. In the ruthenium red procedure the luminal face of the epithelial cells of the nephron was coated distinctly with reaction product. The results obtained revealed that some of the differences at various levels of the nephron depended on the pH values. In glomeruli and proximal convoluted tubules the optimum pH value was 7.4; in the ascending limb of Henle loops and distal convoluted tubules the optimum pH value was 6.8. The ruthenium red-positive surface coat was either closely connected with, or appeared as a part of, the outer leaflet of the unit membrane. The slit pores of glomeruli were also covered by a coat continuous with the surface coat of the adjacent foot processes. The coat lining the microvilli of proximal convoluted tubules completely filled the intervillous spaces. Also, both the colloidal iron method and the colloidal thorium method evidenced the presence of surface coat. Pre-treatment with neuraminidase abolished the effect of the Hale reaction. These results may indicate that the surface coat of the epithelia of the nephron shows the presence of glycoproteins containing siliac acid residues.

Animals↗

PubMed2002

Aminoglycoside and glycopeptide renal toxicity in intensive care patients studied by proton magnetic resonance spectroscopy of urine.

OBJECTIVE: Aminoglycoside and glycopeptide antibiotics are responsible for renal toxicity. In most cases, the nephrotoxicity is limited to a reversible tubular injury, but an acute and sustained renal failure may occur. The aim of our study was to explore the renal function of patients given these antimicrobial agents with proton magnetic resonance spectroscopy of urine. This technique is able to detect, in urine samples, a wide range of metabolites reflecting renal tubular function. The variables assessed by magnetic resonance spectroscopy were compared with the routine markers of renal function: creatinine, urea, and 24-hr urine volume. DESIGN: Prospective clinical study. SETTING: Intensive care unit. PATIENTS: All patients in an intensive care unit receiving an aminoglycoside and/or a glycopeptide were included in the study if they presented with signs of renal dysfunction. All experiments were performed on urine samples collected for the routine follow-up of these patients. INTERVENTION: Proton spectra were acquired with water suppression, and the peak intensity of each metabolite was reported in relationship to the intensity of the creatinine peak. MEASUREMENTS AND MAIN RESULTS: The ratio values obtained by magnetic resonance spectroscopy were compared with the values of creatininemia and blood urea obtained routinely by biochemistry and with the value of the 24-hr urine volume by logistic regression and general linear models. This statistical analysis showed that the ratio of dimethylamine to creatinine was highly correlated with creatininemia. CONCLUSIONS: Dimethylamine is an osmolyte released from the medullar region of the kidney. Thus, our study demonstrated that nephrotoxicity from aminoglycosides and glycopeptides is not limited to proximal tubular toxicity but also may involve the medullar region (Henle loop and collecting duct) of the nephron.

Adult↗

PubMedDate not supplied

Effects of the calcium antagonist nicardipine on renal function and renin release in dogs.

The effects of nicardipine, classed as a calcium antagonist, on renal hemodynamics, renal function, and renin release were investigated in pentobarbital-anesthetized dogs. Intrarenal infusion of this drug at a rate of 5 micrograms/min in both hydrated and hydropenic dogs resulted in a significant increase in renal blood flow, glomerular filtration rate, urine flow, and renin release, with a significant fall in systemic blood pressure. The intrarenal blood flow as measured by the microsphere method indicated a greater increase in flow rate in the juxtamedullary than in the superficial area. During nicardipine infusion, free water reabsorption rate (TcH2O) in hydropenic dogs or free water production (CH2O) in hydrated dogs increased in proportion to the urine flow. Neither TcH2O/CH2O nor CH2O/osmolar clearance were significantly changed throughout the experiments. These data suggest that nicardipine did not inhibit sodium transport at the medullary portion of the ascending limb of Henle, and that the increase in GFR might induce an enhancement of the delivery of sodium to the Henle loop. In addition, an intrarenal hemodynamic alteration may be one possible mechanism involved in the diuretic action of nicardipine. Calcium-antagonistic actions of nicardipine may account for the changes in renal parameters.

Animals↗

PubMed2005

Evidence of a dynamic aldosterone-independent distal tubular control of renal sodium excretion in compensated liver cirrhosis.

BACKGROUND AND AIM: In preascitic cirrhosis increased sodium retention occurs in kidney distal tubule in spite of normal aldosterone plasma levels. No clearance technique can dissect the respective contribution to sodium retention exerted by Henle's loop, distal convoluted tubule and collecting duct, so we evaluated proximal and distal tubular sodium handling in preascites during two manoeuvres that temporarily increase aldosterone secretion. METHODS: Ten patients with compensated cirrhosis and nine controls were studied in recumbency, during standing and after dopamine receptor blockade with metoclopramide through: 4 h renal clearances of sodium, potassium, lithium and creatinine; plasma levels of active renin and aldosterone. RESULTS: Whilst comparable in recumbency, aldosterone levels significantly rose during standing and after metoclopramide in both groups. In patients, dopaminergic blockade caused a fall of distal sodium delivery (P < 0.01) but urinary sodium excretion was unchanged because the reabsorbed fraction of distal sodium delivery also fell (P < 0.03). Cirrhotic patients showed the same findings in the passage from recumbency to standing. CONCLUSIONS: In preascitic cirrhosis, the distal tubular segments of the nephron are able to cope with decreases in tubular flow by reducing reabsorption at an aldosterone-independent site (possibly the loop of Henle).

Adult↗

PubMed2000

Renal urea transporters. Direct and indirect regulation by vasopressin.

Urea is the most abundant urinary solute and is excreted in urine at a much higher concentration than in other body fluids. Urea concentration is achieved in the kidney through complex urea movements between blood vessels and renal tubules, which involve facilitated urea transport. Three major urea transporters expressed in the kidney have been cloned, UT-A1, UT-A2 and UT-B1, the first two derived from the same gene by differential transcription. These membrane proteins enable facilitated diffusion of urea through specific parts of the nephron (UT-A) and through renal vasculature (UT-B) in the medulla. UT-A1 is localised in the terminal part of the inner medullary collecting ducts and accounts for the vasopressin-dependent increase in urea permeability of this segment. UT-A2 is found in the descending thin limbs of Henle's loops. UT-B1 is expressed in the endothelium of the descending vasa recta supplying blood to the renal medulla, and in red cells. All three urea transporters are primarily involved in the process of intrarenal urea recycling, which enables the establishment, and prevents the dissipation, of a high concentration of urea in the inner medulla. This is an essential feature for producing a concentrated urine and thus for water economy in mammals. Vasopressin, upon binding to V2 receptors in the inner medullary collecting ducts, increases urea permeability through activation of UT-A1 molecules, thus enabling urea to diffuse into the inner medullary interstitium. Urea then taken up in ascending vasa recta is returned to the inner medulla via UT-A2 and UT-B1 by countercurrent exchange. These latter two urea transporters are not influenced acutely by vasopressin, but UT-A2 expression is markedly increased in the descending thin limbs of the loops of Henle after sustained exposure to vasopressin or its V2 agonist dDAVP. This effect is indirect because vasopressin receptors are lacking in the descending limbs. The acute direct and delayed indirect actions of vasopressin on renal urea transporters will increase medullary urea accumulation and thus the ability of the kidney to conserve water. Atrial natriuretic peptide inhibits the vasopressin-dependent increase in urea permeability in the inner medullary collecting ducts. The interruption of urea recycling probably contributes to the natriuresis. Impairing in this way the capacity of the kidney to concentrate urea enhances its capacity to concentrate sodium in the urine.

Animals↗

PubMed1995

A re-evaluation of the determinants of glomerular filtration rate.

Several factors are potentially able to change the glomerular filtration rate (GFR) and thereby participate in its regulation, but only a few factors seem to be physiologically important. The variable nature of proximal tubular pressure should be recognized as important in the regulation of GFR. It is argued that a distinction should be made between the terms 'autoregulation of GFR' and 'regulation of GFR'. The tubuloglomerular feedback mechanism (TGF) is an important factor for autoregulatory control of GFR. When perturbations result in major increases in tubular flow, the TGF saturates. Proximal tubular pressure then increases and becomes the major factor responsible for the stabilization of GFR. Changes in the proximal reabsorption rate (APR) are important for long-term variations in GFR (regulation of GFR). Small changes in the APR cause near parallel changes in the GFR mainly through the TGF mechanism, while larger changes in the APR cause near parallel changes in the GFR mainly because of the effect on tubular pressure. The hydraulic resistance in the distal nephron segments is an additional factor in regulating GFR, through its effect on proximal tubular pressure. The stimulus to the TGF mechanism also depresses renin release. The resulting local angiotensin II concentration has effects both on the arteriolar resistances and on the APR. The renin-angiotensin system and TGF are therefore considered to be integrated parts of a common control system regulating GFR. According to the hypothesis advocated here, TGF-mediated changes in afferent arteriolar resistance and angiotensin-mediated changes in efferent arteriolar resistance and APR cooperate in counteracting perturbations in proximal tubular pressure and Henle loop flow. However, because of the biphasic proximal effect of angiotensin II, a major unresolved question is whether physiological increases in endogenous local angiotensin II concentrations stimulate or inhibit proximal reabsorption.

Angiotensin II↗

PubMed1991

Renal tubular actions of ANF.

Many of the earliest investigations of the renal effects of atrial natriuretic factor (ANF) pointed to the glomerulus as a major site of the peptide's action. More recently, there have been many reports showing various effects of ANF on renal tubular epithelia, including collecting ducts, thick ascending limbs of Henle's loop, thin limbs of Henle's loops, and proximal tubules. The purpose of this review is to summarize the evidence for renal tubular actions of ANF and analyze it from the perspective of the specialized functions of the individual nephron segments, addressing the question: can renal tubule effects of ANF play a significant role in the precise day-to-day regulation of renal NaCl and water excretion? Based on these considerations, we propose that long-term renal tubular action of ANF may be distinct from its short-term natriuretic effect. The short-term action of ANF to accelerate salt and water excretion may play a role in the overall response to acute volume overload. This action of ANF appears to be largely due to an ANF-mediated increase in glomerular filtration rate accompanied by a blunting of the tubuloglomerular feedback mechanism, perhaps with some contribution from ANF-mediated inhibition of fluid absorption in the proximal tubule. In contrast, contributions of ANF to the precise day-to-day regulation of salt and water excretion are likely to be chiefly due to ANF-mediated inhibition of NaCl and water absorption in collecting ducts, but may also involve actions of ANF on the loop of Henle.

Animals↗

PubMed1976

Single-nephron function and renal oxygen consumption during rapid volume expansion.

Isotonic volume expansion reduces net filtrate reabsorption in the proximal tubule while increasing it in Henle's loop. To determine the role oxidative metabolism plays in these processes, experiments were performed on rats initially hydropenic and then rapidly volume expanded with isotonic Ringer solution. Whole-kidney sodium reabsorption, oxygen consumption, and single-nephron function were measured simultaneously. During volume expansion, net renal sodium reabsorption increased concomitantly with a fall in oxygen consumption and a reduction in proximal tubular absolute filtrate reabsorption. The increase in quantity of nonreabsorbed filtrate delivered into the loop of Henle greatly exceeded the amount excreted in the urine. Thus, filtrate reabsorption by the distal nephron segments increased. These data provide evidence that acute volume expansion reduces oxygen-dependent active solute transport in the proximal tubule. The increase noted in distal nephron sodium reabsorption appears nonoxygen dependent, energized by anaerobic glycolysis or occurring passively.

Animals↗

PubMed1981

Role of deep nephrons and the terminal collecting duct in a mannitol-induced diuresis.

Recollection micropuncture in Munich-Wistar rats was used to study the effects of intravenous hypertonic mannitol infusions on fluid reabsorption by surface nephrons, prior to the bend of Henle's loop of deep nephrons, and along the papillary collecting duct. During mannitol diuresis, single nephron glomerular filtration rate rose significantly in surface nephrons but fell in deep nephrons. Although mannitol increased the delivery of sodium and water to the end of the proximal tubule and to the first portion of the distal tubule of surface nephrons, water and sodium were reabsorbed between these two sites. In deep nephrons, water reabsorption prior to the bend of the loop of Henle was significantly decreased. Absolute sodium delivery to this site was reduced despite a marked decrease in fractional sodium reabsorption prior to the bend. Papillary osmolality was decreased. Renal plasma flow and inner medullary plasma flow (IMPF) increased proportionally. The reduced water extraction prior to the bend of deep nephrons and the decrease in papillary osmolality could have been partly due to a concomitant increase in IMPF and a decrease in sodium delivery to the medulla. The reabsorption of delivered sodium and water by the papillary collecting duct was reduced to a greater extent than could be expected from the increase in sodium delivery.

Absorption↗

PubMed1981

Renal handling of gentamicin by the Munich-Wistar rat.

Free-flow micropuncture studies were performed in the Munich-Wistar rat to determine the nephron sites of gentamicin transport. The rats were infused with radiolabeled gentamicin and were volume-expanded with either isotonic sodium chloride or sodium bicarbonate. The fractional delivery of ultrafilterable gentamicin (FD) out of the superficial proximal tubule averaged 75% in both groups of animals. FD to the superficial distal tubule averaged 58.1 +/- 2.1% in saline-infused and 91.6 +/- 5.3% in bicarbonate-infused animals. FD to Henle's loop was 118.2 +/- 8.8 and 124.3 +/- 8.1% in saline- and bicarbonate-infused animals, respectively. FD to the base and tip of the papilla was not significantly different between the two groups and averaged 97.3 +/- 2.9 and 96.1 +/- 3.0% in the saline-infused and 100.5 +/- 2.6 and 94.3 +/- 2.8% in the bicarbonate-infused animals. FD to the base of the papilla was significantly lower than that to the loop of Henle in both groups. These studies indicate that gentamicin undergoes net reabsorption in juxtamedullary proximal tubules. Expansion of the extracellular fluid volume with saline or bicarbonate results in differing rates of gentamicin delivery to the superficial distal tubule but not to the base of the papilla. These findings suggest a significant degree of nephron heterogeneity for gentamicin transport in the rat kidney.

Animals↗

PubMed1990

Tubuloglomerular feedback kinetics in spontaneously hypertensive and Wistar-Kyoto rats.

The steady-state behavior of the tubuloglomerular feedback system has been studied in detail, but little is known about its dynamics. However, kinetic data can provide insight regarding the contribution of feedback to autoregulatory responses. Accordingly, experiments were conducted in anesthetized, euvolemic, spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats to characterize the time course of changes in proximal tubular stop-flow pressure after step changes in the rate of orthograde perfusion of Henle's loop. We studied the responses both to increase in perfusion rate, which produced preglomerular vasoconstriction, and decreases in perfusion rate, which produced preglomerular vasodilation. In both strains, the pattern of induced stop-flow pressure transients consisted of a pure delay followed by a monoexponential decay to a new steady state. In SHR rats, delay times were shorter than in WKY rats, but response time constants were not significantly different in the two strains. However, response time constants for dilation were longer than for constriction in both strains. The delay times and relatively large response time constants observed indicate that tubuloglomerular feedback cannot mediate rapid autoregulatory responses to fluctuations in renal perfusion pressure. The response time of tubuloglomerular feedback is probably limited by both the time lag associated with fluid transit through the loop of Henle and a relatively slow rate-limiting step in the signal transduction process at the macula densa.

Animals↗

PubMed2001

Cellular localization of divalent metal transporter DMT-1 in rat kidney.

We have demonstrated that the kidney plays an important role in iron balance and that metabolically significant reabsorption of this ion occurs in the loop of Henle and the collecting ducts [Wareing M, Ferguson CJ, Green R, Riccardi D, and Smith CP. J Physiol (Lond) 524: 581-586, 2000]. To test the possibility that the divalent metal transporter DMT1 (Gunshin H, Mackenzie B, Berger UV, Gunshin Y, Romero MF, Boron WF, Nussberger S, Gollan JL, and Hediger MA. Nature 388: 482-488, 1997) could represent the apical route for iron entry in the kidney, we raised and affinity-purified an anti-DMT-1 polyclonal antibody and determined DMT-1 distribution in rat kidney by Western analysis, immunofluorescence, and confocal microscopy. The strongest DMT1-specific (i.e., peptide-protectable) immunoreactivity was found in the collecting ducts, in both principal and intercalated cells. Thick ascending limbs of Henle's loop and, more intensely, distal convoluted tubules exhibited apical immunostaining. Considerable intracellular DMT-1 immunoreactivity was seen throughout the nephron, particularly in S3 segments. The described distribution of DMT-1 protein is in agreement with our previous identification of nephron sites of iron reabsorption, suggesting that DMT-1 provides the molecular mechanism for apical iron entry in the distal nephron but not in the proximal tubule. Basolateral iron exit may be facilitated by a different system.

Animals↗

PubMed1997

Adenosine and tubuloglomerular feedback.

During the past 16 years numerous studies have shown that adenosine is present in the normoxic kidney and accumulates when ATP hydrolysis prevails over ATP synthesis. Adenosine can induce renal vasoconstriction and a fall in glomerular filtration rate (GFR). The tubuloglomerular feed-back (TGF) mechanism refers to a series of events whereby changes in the NaCl concentration in the tubular fluid at the end of the thick ascending limb of Henle's loop are sensed by the macula densa which then elicits a twofold response in the juxtaglomerular apparatus: a change in the afferent arteriolar tone and GFR and an alteration in renin secretion from granular cells. While an increase in late proximal tubular flow rate, which increases the NaCl concentration and probably transport across the macula densa, lowers GFR and renin secretion, a low NaCl concentration at the macula densa elicits the opposite effects. One important role of the TGF response is to keep the fluid and electrolyte delivery to the distal tubule within certain limits, so that this part of the nephron can accomplish the fine adjustments in reabsorption to meet body needs. In this regard the TGF mechanism serves to establish an appropriate balance between nephron filtration rate and reabsorption in the proximal tubule and loop of Henle. Among several factors, adenosine is considered to be a potential candidate for mediating the TGF response from macula densa to extraglomerular mesangial cells, afferent arteriole, and granular cells. The TGF-mediated vasoconstriction and reduction in renin release following an elevation of the NaCl concentration at the macula densa can be blocked by theophylline and other adenosine-A1-receptor-specific antagonists. Furthermore, the TGF is potentiated by substances that can elevate extracellular adenosine concentrations such as dipyridamole. These and other findings support the concept that adenosine as a metabolic mediator may couple energy metabolism (ATP hydrolysis for tubular Na+ transport) with the control of renin secretion and GFR.

Adenosine↗

PubMed1970

The effect of altered sodium concentration in the distal nephron segments on renin release.

Ethacrynic acid, a potent inhibitor of sodium reabsorption in the ascending limb of Henle's loop, produces a sharp rise in renal venous renin activity within 5 min after intravenous administration in anesthetized dogs. This response persists when volume depletion is prevented by returning urinary outflow to the femoral vein. Comparable studies with chlorothiazide, a diuretic with little or no effect on the medullary portion of the ascending limb of the loop of Henle, failed to produce a significant increase in renal venous renin activity.When administered during ureteral occlusion, ethacrynic acid produced no change in renal venous renin activity until ureteral occlusion was released and flow restored. Following release of the ureters, a prompt rise in renal venous renin was again observed within 5 min of release. Control studies of ureteral occlusion yielded a fall in renal venous renin activity following release of the ureter without administration of ethacrynic acid. These studies identify a prompt stimulatory effect of ethacrynic acid on renin release that is unrelated to volume depletion but dependent upon the presence of tubular urine flow. Although further definition of the site and characteristics of the distal tubular mechanism for stimulation of renin release requires more direct study, the data presented here indicate that changes in sodium concentration in distal tubular fluid serve as a stimulus for renin release.

Angiotensin II↗

PubMed1978

Further studies on segmental sodium transport in the rat kidney during expansion of the extracellular fluid volume.

The present studies were designed to further investigate the possibility of heterogeneity of nephron function during Ringer loading in the rat, and to determine the specific nephron segment responsible for this finding. As in previous studies from this laboratory with smaller rats (50-125 g), net addition of sodium between late distal tubule and papillary base (6.9 vs. 10.4% of the filtered load, respectively, P <0.005) was found in more mature rats (170-230 g). In contrast, there was net reabsorption of sodium between these two segments in nonvolume-expanded animals, 1.70 vs. 0.45% of the filtered sodium load, P <0.005. Because nephron heterogeneity of sodium transport during extracellular volume expansion is the most likely explanation for these findings, further studies were performed to determine the specific juxtamedullary nephron segment responsible for the net addition pattern between late distal tubule and papillary base in Ringer-loaded animals. First, a comparison was made of sodium delivery to the late proximal tubule of superficial nephrons vs. the delivery rate to the bend of Henle's loop of juxtamedullary nephrons in both hydropenia and Ringer loading. Fractional sodium delivery was quite comparable between the superficial and juxtamedullary nephrons in both hydropenia and Ringer loading although the absolute level was much greater in both groups of nephrons in the Ringer studies. Chlorothiazide (15 mg/kg loading and 15 mg/kg per h) given during Ringer loading markedly increased late distal sodium delivery, 19% of the filtered load, but did not prevent net addition of sodium at the papillary base. In contrast, furosemide (5 mg/kg loading and 5/mg/kg per h) given during Ringer loading completely reversed the segmental pattern, 35.5 and 28.8% at late distal tubule and papillary base, respectively, P <0.005. These studies demonstrate that the net addition of sodium between late distal tubule and papillary base during Ringer loading is not limited to immature rats and that the segmental pattern does not occur in non-volume-expanded animals. Further, the reversal of the net addition pattern with furosemide, but not chlorothiazide, and the comparable proximal nephron delivery rates in Ringer loading suggest that the loop of Henle of juxtamedullary nephrons reabsorbs less sodium than the same portion of superficial nephrons in this setting. A model is proposed to explain this finding.

Animals↗