Stimulation of proximal tubular sodium reabsorption by ile5 angiotensin II in the rat kidney

1979 ◽  
Vol 381 (1) ◽  
pp. 83-85 ◽  
Author(s):  
P. J. Harris
Keyword(s):  
Angiotensin Ii ◽  
Rat Kidney ◽  
Sodium Reabsorption ◽  
Tubular Sodium Reabsorption ◽  
Proximal Tubular ◽  
Stimulation Of

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.

Mechanism of prostaglandin E2-induced increase of proximal sodium reabsorption in the rat

1990 ◽  
Vol 258 (1) ◽  
pp. R82-R86 ◽  
Author(s):  
Y. Kinoshita ◽  
F. G. Knox
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Rat Kidney ◽  
Sodium Reabsorption ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Convoluted Tubules ◽  
Stimulation Of ◽  
Interstitial Infusion

Prostaglandin E2, when infused directly into the renal interstitium, enhances sodium reabsorption by the superficial proximal convoluted tubules of anesthetized Sprague-Dawley rats. The present study was designed to investigate the role of angiotensin II in the prostaglandin E2-induced stimulation of proximal sodium reabsorption. Micropuncture at the superficial late proximal tubule demonstrated a significant increase in the fractional reabsorption of sodium from 39.9 +/- 2.3% in control conditions to 51.8 +/- 3.0% (n = 9, P less than 0.01) during the renal interstitial infusion of prostaglandin E2. The stimulatory effect of prostaglandin E2 on proximal sodium reabsorption was markedly attenuated by pretreatment with saralasin. During intravenous saralasin infusion, prostaglandin E2 did not significantly change the fractional reabsorption of sodium from 42.2 +/- 5.8 to 45.4 +/- 6.0% (n = 7, NS). In summary, the stimulatory effect of renal interstitial infusion of prostaglandin E2 on proximal sodium reabsorption was attenuated by pretreatment with saralasin. Therefore renal interstitial infusion of prostaglandin E2 may enhance proximal sodium reabsorption, at least in part, through stimulation of angiotensin II production in the rat kidney.

Crosstalk between the renal sympathetic nerve and intrarenal angiotensin II modulates proximal tubular sodium reabsorption

2015 ◽  
Vol 100 (5) ◽  
pp. 502-506 ◽  
Author(s):  
Roberto B. Pontes ◽  
Adriana C. C. Girardi ◽  
Erika E. Nishi ◽  
Ruy R. Campos ◽  
Cássia T. Bergamaschi
Keyword(s):  
Angiotensin Ii ◽  
Sympathetic Nerve ◽  
Sodium Reabsorption ◽  
Renal Sympathetic Nerve ◽  
Tubular Sodium Reabsorption ◽  
Proximal Tubular ◽  
Renal Sympathetic

Distal tubular sodium reabsorption in the developing rat kidney

1981 ◽  
Vol 240 (6) ◽  
pp. F487-F491 ◽  
Author(s):  
A. Aperia ◽  
G. Elinder
Keyword(s):  
Rat Kidney ◽  
Age Groups ◽  
Distal Tubule ◽  
Sodium Reabsorption ◽  
Tubular Sodium Reabsorption ◽  
Saline Loading ◽  
Proximal Tubular ◽  
Old Rats ◽  
Developing Rat

The immature kidney has a blunted natriuretic response to saline loading. to localize the high fractional Na reabsorption in the developing nephron, we determined Na delivery to the early distal tubule (EDT) and the fraction of filtered Na remaining in the tubular fluid [(TF/P)Na/In] in the EDT and late distal tubule (LDT) in 24- and 40-day-old hydropenic (HP) and volume-expanded (VE) rats. During HP the (TF/P)Na/In ratio in EDT was significantly higher in the younger rats (12.6 +/- 2.0%) than in the older rats (4.2 +/- 0.6%), but because of a lower SNGFR in the younger rats th Na delivery to EDT was the same in both age groups. The (TF/P)Na/In ratio in LDT was not different in 24- and 40-day-old HP rats (1.1 +/- 0.4 and 1.7 +/- 0.3%, respectively). During VE th (TF/P)Na/In ratio in LDT was significantly lower in 24- (3.0 +/- 0.7%) than in 40-day-old rats (8.3 +/- 1.1%). The (TF/P)Na/In ratio in LDT correlated well with the urinary fractional Na excretion. It is concluded that the Na reabsorption capacity of the developing nephron is more efficient in the distal tubule than in the more proximal tubular segments.

Inhibition of distal tubular sodium reabsorption by angiotensin II

1963 ◽  
Vol 205 (1) ◽  
pp. 133-138 ◽  
Author(s):  
Arthur J. Vander
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Sodium Concentration ◽  
Relative Increase ◽  
Sodium Reabsorption ◽  
Left Renal Artery ◽  
Tubular Sodium Reabsorption ◽  
Proximal Tubular ◽  
The Right ◽  
Stop Flow

Angiotensin II or norepinephrine was infused directly into the left renal artery of anesthetized dogs undergoing mannitol diuresis, and the right and left kidneys were compared for GFR (Ccr or Cin), RPF (Cpah), sodium excretion, and distal stop-flow sodium and inulin patterns. Both angiotensin and norepinephrine caused similar reductions of GFR and RPF on the left, as compared with the right, but only angiotensin prevented normal lowering of left distal stop-flow sodium concentration, even when length of occlusion was 14 min. The minimum effective dose was 6–12 mµg/kg min, and maximal differences between left and right sodium minima occurred with 50 mµg/kg min. Distal inulin patterns were not altered by angiotensin, nor were "postocclusive" inulin patterns. Clearance data demonstrated that when GFR changes were taken into account angiotensin caused a relative increase in sodium excretion compared to control or norepinephrine-infused dogs. These stop-flow and clearance data support the hypothesis that angiotensin inhibits distal sodium reabsorption by a direct tubular effect. No attempt was made to evaluate possible effects of angiotensin on proximal tubular sodium reabsorption.

Increased Proximal Tubular Sodium Reabsorption in Hypertensive Patients with Type 2 Diabetes

1989 ◽  
Vol 6 (7) ◽  
pp. 614-620 ◽  
Author(s):  
J.-C. Mbanya ◽  
T. H. Thomas ◽  
R. Taylor ◽  
K. G. M. M. Alberti ◽  
R. Wilkinson
Keyword(s):  
Type 2 Diabetes ◽  
Sodium Reabsorption ◽  
Hypertensive Patients ◽  
Tubular Sodium Reabsorption ◽  
Proximal Tubular
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