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Query: UNIPROT:Q92565 (GFR)
 4,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of sodium nitrate were compared with sodium chloride loading on transport of electrolytes by the nephron. Maximal levels of free water clearance/clomerular filtration rate (CH2O/GFR) averaged 8.4% with nitrate loading and 14.4% with saline loading. Since ethacrynic acid and chlorothiazide exert their major natriuretic effect in the distal nephron, the increment in Na ad Cl reabsorbed beyond the proximal tubule. The administration of these agents resulted in an increase in fractional sodium excretion (CNa/GFR) of 21.1%, urinary sodium excretion (UNaV) of 1,126 mueq/min, and urinary chloride excretion (UClV) of 848 mueq/min during nitrate loading compared with an increase in CNa/GFR of 37.6%, UNaV of 2,362 mueq/min, and UClV of 2,397 mueq/min during saline loading. The smaller diuretic-induced increment in Na and Cl excretion in the nitrate studies suggests, as do the hydrated studies, that less Cl and Na are reabsorbed in the distal nephron during nitrate than saline loading. At every level of UNaV, fractional bicarbonate reabsorption was higher, urine pH was lower, and urinary potassium excretion (UKV) was higher in the nitrate studies. Thus, compared with saline loading, sodium nitrate decreases chloride and sodium reabsorption in the distal nephron. The higher hydrogen and potassium secretion in the nitrate studies may be consequent to the decreased ability of the distal nephron to reabsorb chloride.
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PMID:Effect of sodium nitrate loading on electrolyte transport by the renal tubule. 0 16

The purpose of this study was to clarify the means by which lithium induced a disorder of urine acidification. Rats infused with hydrochloric acid (1 mEq/kg) developed acute metabolic acidosis (blood Ph = 7.32; bicarbonate, 18 mEq/liter) with a urine pH of approximately 5.85. The addition of lithium chloride (4 mEq/kg i.p) caused an increase in the urine pH (6.38) and a further decrease in blood bicarbonate (11.0 mEq/liter). During bicarbonate loading, lithium caused the urine PCO2 to fall significantly (urine minus blood PCO2 decreased from 25.3 +/-2.8 To 14.4 +/- 2.3 mm Hg) These changes were not seen following equimolar i.p. administration of sodium chloride. Similarly, lithium administration depressed bicarbonate reabsorption by 11.1% (from 30.6 to 27.2muEq/ml of GFR) during alkali infusion, while saline caused only a 5% decrease (30.0 to 28.5muEq/ml of GFR). The combination of an increase in urine PCO2 in alkaline urine indicates that lithium produced a defect in distal nephron hydrogen ion secretion. The fall in bicarbonate reabsorption following lithium administration oculd be due to a mild hydrogen ion secretory defect located in the proximal tubule or a severe defect in the distal nephron.
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PMID:Lithium-induced impairment of urine acidification. 0 8

1. The effects of sodium DL-lactate and sodium chloride (2.5 mg/kg as 865 mmol/l solutions given by intravenous infusion over 20 min) on the renal tubular reabsorption of phosphate have been compared in five normal adults. 2. Sodium lactate produced a marked but transient increase in urinary phosphate excretion due to a reduction in net renal tubular reabsorption of phosphate; the mean value of the maximum rate of renal tubular reabsorption of phosphate/unit of glomerular filtration rate (TmP/GFR) decreased from 1.14 to 0.82 mmol/l. 3. This effect was not due simply to expansion of the volume of the extracellular fluid, since the reduction in TmP/GFR after sodium chloride infusion was less marked, nor did it seem to be due entirely to alkalinization of the urine since the maximum increase in urinary pH occurred 20--40 min after the maximum decrease in TmP/GFR.
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PMID:Effect of intravenous sodium lactate on renal tubular reabsorption of phosphate in man. 3 39

Total kidney GFR's, urine flow, inorganic ion excretion, and single nephron glomerular filtration rates (SNGFRs) were evaluated in anesthetized starlings under control conditions (2.5% mannitol infusion) and in starlings subjected to an osmotic stress induced by the intravenous infusion of 5.8% sodium chloride. Under control conditions the GFR was 2.92 ml/kg per min, urine flow 0.20 ml/kg per min, 63% of filtered sodium was reabsorbed, mean mammalian type (MT) SNGFR was 15.6 nl/min, and mean reptilian type (RT) SNGFR was 7.0 nl/min. During osmotic stress the GFR did not change, urine flow increased to 3 times the control level, the percentage of filtered sodium reabsorbed did not change, both the mean MT SNGFR (24.3 nl/min) and the mean RT SNGFR (10.3 nl/min) were significantly higher than the control levels. During the osmotic stress more MT and fewer RT nephrons were filtering than during control conditions. Under control conditions 98.5% of the sodium excreted by the kidney was associated with uric acid. This percentage decreased as the osmotic stress increased. The starlings tended to excrete the osmotic load imposed by the infusion of NaCl to prevent the plasma osmolality from increasing.
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PMID:Renal response of the starling (Sturnus ;ulgaris) to an intravenous salt load. 64 62

A total of 45 infants were studied on the fourth or fifth day of life: 13 term and 10 pre-term infants with serum bilirubin levels ranging between 257 and 390 mumol/l were compared with 12 term and 10 pre-term infants with serum bilirubin levels below 195 mumol/l. The groups did not differ with regard to mean gestational age or mean post-natal age. GFR and CPAH were determined with the single injection clearance method and ability to excrete Na+ was determined following an oral loading of sodium chloride. GFR was lower in infants with hyperbilirubinemia and correlated negatively to the highest recorded serum bilirubin value. CPAH was similar in hyperbilirubinemic infants and controls. The urinary sodium excretion was significantly higher in infants with hyperbilirubinemia.
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PMID:Renal function in infants with hyperbilirubinemia. 75 31

To determine if an increase in the endogenous secretion of parathyroid hormone could decrease sodium reabsorption by the proximal tubule, the ionized calcium concentration of blood perfusing the parathyroid gland of eight unilaterally thyroid parathyroidectomized dogs (TPTX) was reduced by infusion of an isotonic sodium citrate plus sodium chloride solution into the blood supply of the parathyroid gland. The fractional clearance of phosphate increased significantly (+9.3 +/- 2.8 ml/min per 100 ml GFR), while fractional sodium reabsorption by the proximal tubule decreased (-.06 +/- .02; P less than .025). In seven normal control dogs that received isotonic sodium chloride infusion, neither fractional sodium reabsorption by the proximal tubule nor the fractional clearance of phosphate was significantly altered. In five bilaterally TPTX dogs that received a sodium citrate plus sodium chloride infusion, sodium reabsorption by the proximal tubule was not significantly altered. There were no significant changes in glomerular filtration rate or renal plasma flow in any of these groups. The data demonstrate that alterations in endogenous parathyroid hormone secretion can play a significant role in the regulation of sodium reabsorption by the proximal tubule.
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PMID:Effect of parathyroid hormone secretion on sodium reabsorption by the proximal tubule. 120 Jan 36

Bicarbonate reabsorption in the thick ascending limb of Henle's loop was examined by studies of free-water clearance (CH2O) and free-water reabsorption (TcH2O). During maximal water diuresis in the dog, CH2O/GFR was taken as an indes of sodium reabsorption in, and urine flow (V/GFR) as an index of delivery of filtrate to, this scarbonate, infusion of a nonreabsorbable solute (hypotonic mannitol) and administration of an inhibitor of bicarbonate reabsorption (acetaent, but less than that achieved with hypotonic saline infusion. This suggests that sodium that sodium bicarbonate is not reabsorbed in the ascending limb. Rather, it is the sodium chloride, swept out of the proximal tubule by osmotic diuresis due to nonreabsorbed mannitol or sodium bicarbonate, that is reabsorbed in the ascending limb thereby increasing CH2O, whereas the nonreabsorption of mannitol and sodium bicarbonate results in a depressed CH20 per unit V when compared with hypotonic saline. V/GFR is not a satisfactory index of delivery to the ascending limb during osmotic diuresis, since it includes water obligated by nonreabsorbable solutes. When a better index of delivery, the sum of the clearances of chloride (CC1) and free-water (CH2O) is used, hypotonic bicarbonate infusion, hypotonic mannitol infusion and acetazolamide administration increase CH2O/GFR per unit delivery to the same extent as odes hypotonic saline infusion. Studies in dogs and rats on TcH2O also indicate that sodium bicarbonate is an impermeant solute in the ascending limb. Osmotic diuresis due to sodium bicarbonate diuresis, produced either by inhibition of sodium bicarbonate reabsorption (acetazolamide, L-lysine mono-hydrochloride) or infusion of sodium bicarbonate, or mannitol diuresis both produced marked chloruresis and increased TcH2O to the same extent as did hypertonic saline infusion. If chloride excretion was almost eliminated by hemodialysis against a chloride-free dialysate (dogs) or prolonged feeding of a salt-free diet (rats), TcH2O formation was unimpaired if hypertonic saline was infused but virtually obliterated during mannitol or sodium bicarbonate diuresis. Sodium reabsorption in the ascending limb, therefore, appears to be dependent upon chloride as the accompanying anion. At any given rate of bicarbonate excretion, more cloride is delivered out of the proximal tubule (as estimated from CC1 + CH2O) with hypotonic sodium bicarbonate infusion than with acetazolamide administration. This suggests that magnitude of the chlorutesis accompanying bicarbonate diuresis depends, not only on osmotic diuresis due to nonreabsorbed sodium bicarbonate, but also on the extent to which concomitant changes in effective extracellular volume influence overall sodium chloride reabsorption.
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PMID:Evidence against bicarbonate reabsorption in the ascending limb, particularly as disclosed by free-water clearance studies. 120 62

Renal function was studied in anesthetized starlings by micropuncture and clearance techniques. The effects of intravenous infusions of isosmotic sodium chloride and hyposmotic mannitol solutions were compared. In the proximal tubules of the superficial reptilian-type nephrons, there is net reabsorption of sodium, chloride, and potassium; net secretion of calcium and urate; and either net secretion or no net secretion or reabsorption of magnesium and phosphate. The fractional delivery of ions and urate to the site of micropuncture, the percent of fluid reabsorbed, and the single nephron glomerular filtration rate (SNGFR) were not significantly different between the two infusion treatments. However, in the sodium chloride-infused birds, whole kidney GFR and the fractional excretion of sodium and chloride by the whole animal were higher, and fractional excretion of magnesium and potassium were lower. The data for each infusion group were further subdivided on the basis of whether the birds were in molt. In starlings, molt is associated with elevated levels of plasma prolactin. For the sodium chloride infusion, sodium and water reabsorption to the site of micropuncture was greater in the birds in molt than in those not in molt.
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PMID:Micropuncture study of the avian kidney: infusion of mannitol or sodium chloride. 210 46

Renal tubular sodium and water handling determined by the lithium clearance technique, plasma concentrations of atrial natriuretic peptide (ANP), angiotensin II, aldosterone, arginine vasopressin (AVP), and urinary excretion of prostaglandin E2 (PGE2) were determined both during basal conditions and before and after intravenous sodium loading with a 2.5% sodium chloride solution in patients with polycystic kidney disease (PKD), ten with normal or slightly reduced kidney function (PKDN) and seven with moderately reduced kidney function (PKDR), and in 15 healthy controls. In PKDN tubular function was normal, whereas in PKDR both proximal and distal reabsorption of sodium and water were reduced. Angiotensin II and aldosterone were normal in both groups of patients. During basal conditions ANP was higher in PKDR than in PKDN. PGE2 was significantly higher in PKDR than in PKDN. For all patients significant correlations were found between GFR and both ANP (rho = -0.51, n = 17, P less than 0.05) and PGE2 (rho = -0.53, n = 17, P less than 0.05). It is concluded that renal sodium handling is normal in the early stages of PKD. With deterioration of kidney function both proximal and distal tubular reabsorption of sodium is reduced and the accompanying changes in ANP and PGE2 may be compensatory phenomena counteracting declining glomerular filtration rate.
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PMID:Change in renal tubular sodium and water handling during progression of polycystic kidney disease: relationship to atrial natriuretic peptide. 214 89

To examine whether plasma growth hormone is necessary for the amino acid-induced rise in effective renal plasma flow (ERPF, PAH clearance) and GFR (inulin clearance), arginine HCl, 500 mg/kg, was infused for 30 minutes into eight normal and six growth hormone-deficient individuals. During infusion, ERPF increased in the normal and growth hormone-deficient subjects by 28.9 +/- 11.4 SD-% (P less than 0.01) and 46.5 +/- 14.4% (P less than 0.001). GFR rose by 23.7 +/- 5.9% (P less than 0.05) and 42.7 +/- 29.1% (P less than 0.001) in the two groups. Plasma growth hormone rose only in the normal subjects, while glucagon increased in both groups. Infusion of arginine HCl, 200 mg/kg, into normals increased ERPF and GFR without increasing plasma osmolality. Lower arginine doses essentially did not affect ERPF, GFR, growth hormone, or glucagon. Infusion of D-glucose into normals raised plasma osmolality as high as with arginine HCl, 500 mg/kg, but increased ERPF only slightly and not GFR; D-glucose infusion caused a delayed rise in growth hormone that was unassociated with an increase in ERPF or GFR. An infusion of ammonium chloride with sodium chloride, which provided an amount of chloride similar to the 500 mg/kg arginine HCl dose, did not change ERPF and GFR; this suggests that the chloride load did not cause the altered renal hemodynamics stimulated by arginine HCl. These findings indicate that neither normal plasma growth hormone levels nor a rise in growth hormone mediates the arginine-induced acute increase in ERPF or GFR. This effect is also not due to the osmolar load but could be caused by the rise in plasma glucagon.
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PMID:Role of growth hormone in the amino acid-induced acute rise in renal function in man. 366 97


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