Micropuncture study of handling of phosphate by proximal and distal nephron in normal and parathyroidectomized rat. Evidence for distal reabsorption

Section: Statisticssupporting

confidence: 71%

P-31 nuclear magnetic resonance spectroscopic study of obstructive uropathy in the rat.

Shapiro¹,

Chan²

1987

“…However, since there is a rather normal entry of molecules in the proximal tubule, this efflux can be partially or totally corrected downstream. At the distal nephron, this is not the case: there is no absorption of amino acids (9) and absorption of phosphate is rather small (38,39) or nonexistent (40,41); therefore, the molecules that exit at this site are excreted directly into the urine. This explains the modification in the urinary outflow pattern seen in our stop-flow experiments (Figs.…”

Section: Introductionmentioning

confidence: 99%

Membrane permeability as a cause of transport defects in experimental Fanconi syndrome. A new hypothesis.

Bergeron¹,

Dubord²,

Hausser³

et al. 1976

A B S T R A C T The injection of sodium maleate (200-400 mg/kg) into rats produces aminoaciduria along with glycosuria and phosphaturia, resembling the Fanconi syndrome. This experimental model was studied by means of microinjections into proximal convoluted tubules of the kidney, stop-flow diuresis, and microperfusion of single nephrons. Our results show that, in maleate-treated rats, competition between amino acids of related structures (L-proline, L-OH-proline, and glycine) possesses the same characteristics, and net influx of amino acids appear normal at the proximal nephron. Data obtained by classical stop-flow techniques and single nephron microperfusions also indicate a normal entry of labeled amino acids (L-lysine, glycine, L-valine, L-proline, L-cystine), and 3-0-methyl-D-[3H]glucose and ['P]phosphate from the luminal side of the proximal tubule cell. However, the efflux of molecules from the cell appears enhanced throughout the proximal and distal tubule; molecules that exit at this site are excreted directly into the urine. Our results suggest that the phosphaturia, aminoaciduria, and glycosuria of the experimental Fanconi syndrome can be explained by a modification of the cell membrane permeability (increased efflux) at distal sites of the nephron rather than by a modification of the membrane transport (decreased influx) at the proximal sites, as is currently accepted. Our data also stress the importance of efflux phenomena in membrane transport.

“…Recent micropuncture studies have demonstrated several important features of the renal reabsorptive process for inorganic phosphate (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). First, the proximal tubule is responsible for most but not all of phosphate reabsorption, the most avid site being the early portion of the proximal convoluted tubule (2,4).…”

Section: Introductionmentioning

confidence: 99%

“…First, the proximal tubule is responsible for most but not all of phosphate reabsorption, the most avid site being the early portion of the proximal convoluted tubule (2,4). Second, phosphate reabsorption has been found to parallel fluid reabsorption in the proximal tubule under certain experimental conditions (5)(6)(7)(8)(9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

A Microperfusion Study of Phsophate Reabsorption by the Rat Proximal Renal Tubule EFFECT OF PARATHYROID HORMONE

Bank¹,

Aynedjian²,

Weinstein³

1974

A B S T R A C T To study the mechanism of phosphate reabsorption by the proximal tubule and the effect of parathyroid hormone (PTH), microperfusion experiments were carried out in rats. Segments of proximal tubule isolated by oil blocks were perfused in vivo with one of three solutions, each containing 152 meq/liter Na' and 2 mmol/liter phosphate, but otherwise differing in composition. The pH of solution 1 was 6.05-6.63, indicating that 60-85% of the phosphate was in the form of H2PO4. The pH of solution 2 was 7.56-7.85, and 85-92% of the phosphate was in the form of HP04=. Solution 3 contained HC03-and glucose and had a pH of 7.50-7.65. When the proximal tubules were perfused with solution 1, the "2P concentration in the collected perfusate was found to be consistently lower than in the initial perfusion solution. In sharp contrast, when the tubules were perfused with solutions 2 or 3, s'P concentration usually rose above that in the initial solution. Water (and presumably Na') reabsorption, as measured with ['H]inulin, was the same with the acid and alkaline solutions. Administration of partially purified PTH clearly prevented the fall in phosphate concentration with the acid solution, but had a less discernible effect on phosphate reabsorption with the two alkaline solutions. Measurements of pH within the perfused segments with antimony microelectrodes demonstrated that PTH enhanced alkalinization of the acid perfusion solution. The findings are consistent with the view that H2POf is reabsorbed preferentially over HPO4=. This can be attributed to either an active transport mechanism for H2PO4J or selective membrane permeability to this anion. PTH appears to either inhibit an active transport process for H2PO4-, or to interfere with pas-