Proximal tubular transport and urinary excretion of sodium after renal denervation in sodium depleted rats

1985 ◽  
Vol 403 (2) ◽  
pp. 146-150 ◽  
Author(s):  
G�bor Sz�n�si ◽  
P�l Benes�th ◽  
Lajos Tak�cs ◽  
Bozena Asztalos ◽  
M�ria Vedres
Keyword(s):  
Urinary Excretion ◽  
Renal Denervation ◽  
Tubular Transport ◽  
Proximal Tubular

Tubular transport and urinary excretion of phosphate after renal denervation in the anesthetized rat

1981 ◽  
Vol 240 (6) ◽  
pp. F481-F486 ◽  
Author(s):  
G. Szenasi ◽  
P. Bencsath ◽  
E. Lehoczky ◽  
L. Takacs
Keyword(s):  
Urinary Excretion ◽  
Inorganic Phosphate ◽  
Renal Denervation ◽  
Left Kidney ◽  
Tubular Reabsorption ◽  
Male Rats ◽  
Tubular Transport ◽  
Transport Of Inorganic Phosphate ◽  
Chronic Denervation ◽  
Two Sides

Tubular transport of phosphate (Pi) was studied using clearance and tracer microinjection techniques in Inactin-anesthetized male rats subjected to left kidney denervation. Experiments were conducted in the following groups: i) acute denervation (AD); ii) chronic denervation (CD); iii) acute denervation plus thyroparathyroidectomy (AD + TPTX); iv) microinjection with AD. Besides a marked diuresis and natriuresis with no difference in GFR between innervated (inn) and denervated (den) kidneys, unilateral renal denervation resulted in an increased urinary excretion and decreased tubular reabsorption of inorganic phosphate. Maximum tubular reabsorption of Pi (TmPi) calculated per unit GFR was (means +/- SE): AD, inn: 2.38 +/- 0.04, den: 1.98 +/- 0.06 mumol/ml; CD, inn: 2.66 +/- 0.10, den: 2.19 +/- 0.11 mumol/ml; AD + TPTX, inn: 4.78 +/- 0.06, den: 4.26 +/- 0.08 mumol/ml. Thus, differences in TmPi between the two sides were of the same magnitude in the three groups. Fractional recovery of 32Pi from microinjections in control (C) and postdenervation (D) periods was: early proximal, C: 53.0 +/- 0.81, D: 61.3 +/- 1.07%; late proximal, C: 77.0 +/- 0.81, D: 70.6 +/- 0.60%; early distal, C: 93.7 +/- 0.75, D: 03.5 +/- 0.72%. It is concluded that renal sympathectomy depresses tubular transport of inorganic phosphate in anesthetized rats by a primary action on the proximal convoluted tubule and with a partial compensation in the loop of Henle.

Renal nerves and postprandial renal excretion in the conscious monkey

1991 ◽  
Vol 261 (5) ◽  
pp. R1197-R1203 ◽  
Author(s):  
T. V. Peterson ◽  
B. A. Benjamin ◽  
N. L. Hurst ◽  
C. G. Euler
Keyword(s):  
Urinary Excretion ◽  
Nonhuman Primate ◽  
Nasogastric Tube ◽  
Sodium Excretion ◽  
Renal Denervation ◽  
Renal Excretion ◽  
Renal Nerves ◽  
Electrolyte Excretion ◽  
Macaque Monkeys ◽  
High Sodium

Experiments were performed in conscious macaque monkeys to determine if the renal nerves are important in mediating postprandial increases in renal fluid-electrolyte excretion in this species. Monkeys were given a high-sodium meal via a nasogastric tube. Consecutive 10-min urine samples were taken during the 30-min time of meal administration and then 180 min postprandially. The experiment was performed both before and 10-14 days after each animal underwent renal denervation. Diuresis and natriuresis occurred under both renal-innervated and -denervated conditions. However, the amounts of urine and sodium excreted were less after renal denervation. For the total 210 min of measurements obtained after the meal was started, cumulative urine output was 95.0 +/- 26.4 ml and sodium excretion 7.18 +/- 1.74 meq in innervated kidneys vs. 56.7 +/- 7.0 ml (a 40% decrease; P less than 0.005) and 4.84 +/- 0.99 meq (a 33% decrease; P less than 0.01) after denervation. These results demonstrate that the renal nerves are important in the nonhuman primate for eliciting the postprandial changes in urinary excretion secondary to intake of a high-sodium meal.

Disorders of tubular electrolyte handling

2020 ◽  
pp. 5112-5123
Author(s):  
Nine V.A.M. Knoers ◽  
Elena N. Levtchenko
Keyword(s):  
Serum Magnesium ◽  
Serum Phosphate ◽  
Magnesium Concentration ◽  
Main Site ◽  
Fanconi’S Syndrome ◽  
Tubular Transport ◽  
Bone Changes ◽  
Proximal Tubular ◽  
Magnesium Excretion ◽  
Fanconi's Syndrome

Glycosuria—glucose reabsorption in the proximal tubule is carried out by two different pairs of apical Na+-dependent (SGLT1 and -2) and basolateral Na+-independent (GLUT1 and -2) glucose transporters. Abnormalities in renal glucose transport can be seen in association with other defects of proximal tubular transport. Familial renal glycosuria is a rare autosomal recessive condition caused by mutations in the SGLT2-encoding gene, SLC5A2. Phosphate-handling disorders—the plasma concentration of inorganic phosphate depends on the balance between intestinal absorption, renal excretion, and the internal contribution from bone. Changes of serum phosphate levels can be caused by numerous inherited and acquired conditions. Disorders associated with increased urinary phosphate excretion and low serum phosphate levels produce symptoms that mainly affect the bones: rickets in children and osteomalacia in adults. Magnesium-handling disorders—normal plasma magnesium concentration is achieved by variation of urinary magnesium excretion in response to altered uptake by the intestine. The main site of magnesium absorption is the small bowel, via paracellular simple diffusion at high intraluminal concentrations, and via active transcellular uptake through the magnesium channel TRPM6 at low concentrations. Regulation and fine-tuning of serum magnesium concentration occurs primarily in the kidney. Genetic disorders of magnesium handling include Gitelman’s syndrome. Aminoaciduria and renal Fanconi’s syndrome—most amino acids (except for tryptophan, which is protein bound) are freely filtered by the glomerulus, after which 95 to 99.9% are reabsorbed in the proximal tubules by apical Na+-dependent cotransporters and Na+-independent cotransporters. Aminoaciduria is defined as urinary excretion of more than 5% of the filtered load of an amino acid. Renal Fanconi’s syndrome is characterized by a generalized defect of both Na+-coupled and receptor-mediated proximal tubular transport.

Effect of renal interstitial infusion of arachidonic acid on proximal sodium reabsorption

1989 ◽  
Vol 257 (2) ◽  
pp. F237-F242 ◽  
Author(s):  
Y. Kinoshita ◽  
J. C. Romero ◽  
F. G. Knox
Keyword(s):  
Arachidonic Acid ◽  
Urinary Excretion ◽  
Proximal Tubules ◽  
Sodium Reabsorption ◽  
Renal Interstitium ◽  
Tubular Sodium Reabsorption ◽  
Proximal Tubular ◽  
The Individual ◽  
Stimulation Of ◽  
Interstitial Infusion

The effect of prostaglandins (PGs) on proximal sodium reabsorption has not been fully defined. The objective of the present study was to determine the response of proximal tubular sodium reabsorption to infusions of arachidonic acid and specific PGs into the renal interstitium in rats. Renal interstitial infusions of arachidonic acid as well as the individual PGs, I2, E2, and F2 alpha, were employed to elevate the concentration of these PGs in the kidney. Infusion of 10(-4) M arachidonic acid elicited a marked increase of urinary excretion of 6-keto-PGF1 alpha (a stable metabolite of PGI2) from 260.1 +/- 52.7 to 507.4 +/- 129.5 pg/min (P less than 0.05) and a smaller increase of PGE2 from 18.4 +/- 11.2 to 25.9 +/- 10.9 pg/min (P less than 0.05). When micropuncture samples were obtained from superficial late proximal tubules, infusion of arachidonic acid increased the fractional delivery of sodium (FDNa) from 47.8 +/- 5.9 to 58.3 +/- 4.6% (n = 6, P less than 0.01). In the presence of indomethacin, arachidonic acid failed to augment FDNa. Infusion of 10(-5) M PGI2 also increased FDNa from 51.4 +/- 3.4 to 64.0 +/- 4.4% (n = 10, P less than 0.01). PGF2 alpha did not change FDNa and PGE2 decreased it from 53.1 +/- 5.4 to 37.4 +/- 3.3% (n = 8, P less than 0.01). In summary, the present study demonstrates that renal interstitial infusion of arachidonic acid decreases sodium reabsorption by the superficial proximal tubules possibly through the stimulation of PGI2 production.

Autoradiographic study of Diodrast-I131 transport in Necturus kidney

1960 ◽  
Vol 199 (5) ◽  
pp. 931-941 ◽  
Author(s):  
William B. Kinter ◽  
Lucian L. Leape ◽  
Jordan J. Cohen
Keyword(s):  
Autoradiographic Study ◽  
Intracellular Concentration ◽  
Tubular Cells ◽  
Different Types ◽  
Tubular Transport ◽  
Proximal Tubular ◽  
Renal Tubular Transport ◽  
Arterial Plasma ◽  
Renal Tubular ◽  
Bidirectional Movement

Renal tubular transport of Diodrast-I131 was studied in Necturus by newly devised autoradiographic methods used in conjuction with classical clearance methods. Clearance measurements on individual animals indicate different types of over-all tubular transport ranging from secretion into tubular urine, heretofore reported in many species, to reabsorption out of tubular urine, so far reported only in Necturus. Diodrast content of tubular urine as disclosed by autoradiography both corroborates clearance data and provides evidence that proximal tubules are the major site of Diodrast transport irrespective of direction. This view is supported by inulin-C14 autoradiographs. In addition, significant amounts of Diodrast were accumulated within proximal tubular cells during all types of transport. With less than 3 mg Diodrast/100 ml arterial plasma, the estimated intracellular concentration ranged from 2 to 19 times that in plasma. At higher plasma levels, tubular transport was overwhelmed and intracellular concentration no longer exceeded that in plasma. These results support a previously formulated theory of simultaneous, bidirectional movement of Diodrast across tubular cells in Necturus kidney.

Increased spillover of dopa into arterial blood during dietary salt loading

1990 ◽  
Vol 78 (4) ◽  
pp. 423-429 ◽  
Author(s):  
Ehud Grossman ◽  
Aaron Hoffman ◽  
Peter C. Chang ◽  
Harry R. Keiser ◽  
David S. Goldstein
Keyword(s):  
Steady State ◽  
Urinary Excretion ◽  
Renal Denervation ◽  
Renal Nerves ◽  
Dietary Salt ◽  
Rat Strains ◽  
Salt Loading ◽  
Arterial Blood ◽  
Daily Excretion ◽  
Excretion Rates

1. We measured urinary excretion rates of dopamine (3,4-dihydroxyphenethylamine) and dopa (3,4-dihydroxyphenylalanine) and the spillover rate of dopa into arterial blood during dietary salt loading in conscious Dahl salt-sensitive and salt-resistant rats with intact or denervated kidneys. 2. Dopa spillover was calculated from the steady-state clearance of intravenously infused l-[3H]dopa and arterial levels of endogenous dopa. 3. Daily excretion rates of dopa and dopamine increased by about sixfold during salt loading in both rat strains. Bilateral renal denervation delayed these increases and the natriuretic responses. 4. During dietary salt loading, dopa spillover increased to approximately the same extent as simultaneously measured dopamine excretion. 5. The results suggest that increases in urinary excretion of dopamine during dietary salt loading can be accounted for by increases in the release of dopa into the bloodstream and that the renal nerves contribute to the dopa and dopamine excretory responses.

Effect of parathyroid hormone on renal tubular permeability

1976 ◽  
Vol 231 (5) ◽  
pp. 1401-1407 ◽  
Author(s):  
WB Lorentz
Keyword(s):  
Parathyroid Hormone ◽  
Active Transport ◽  
Intravenous Infusion ◽  
Rat Kidney ◽  
Tubular Transport ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Tubular Permeability

The effect of parathyroid hormone (PTH) on renal tubular permeability has been studied utilizing micropuncture techniques in the rat kidney. After microinjection into superificial nephrons during control conditions, inulin (98.8 +/- 2.7%) and mannitol (97.2 +/- 2.4%) recovery from the experimental kidney was essentially complete. During intravenous infusion of PTH, inulin (99.3 +/- 2.9%) recovery was again complete. Mannitol recovery decreased signficantly after both early-proximal (84.7 +/- 5.8%, P less than 0.001) and late-proximal (89.7 +/- 2.8%, P less than 0.001) injections. There was no loss of either mannitol or inulin following distal tubular injection. Late-proximal TF/P inulin ratios during control conditions were 2.10 +/- 0.20 and decreased insignificantly to 1.99 +/- 0.21 during PTH infusion. Late-proximal TF/P mannitol rations were 2.09 +/- 0.21 during control periods and during PTH infusion decreased significantly to 1.78 +/- 0.19 (P less than 0.001). These results indicate that PTH induces a change in proximal tubular permeability to a usually impermeable nonelectrolyte, mannitol. The effects of PTH on proximal tubular transport could be partially explained by this alteration in permeability, which would increase passive backflux of actively transported species and decrease net transport while having no effect on active transport.

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