Dose-dependent stimulation and inhibition of proximal tubular sodium reabsorption by angiotensin II in the rat kidney

1977 ◽  
Vol 367 (3) ◽  
pp. 295-297 ◽  
Author(s):  
P. J. Harris ◽  
J. A. Young
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

1981 ◽  
Vol 240 (6) ◽  
pp. F487-F491 ◽  
Author(s):  
A. Aperia ◽  
G. Elinder

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.


1963 ◽  
Vol 205 (1) ◽  
pp. 133-138 ◽  
Author(s):  
Arthur J. Vander

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.


1989 ◽  
Vol 6 (7) ◽  
pp. 614-620 ◽  
Author(s):  
J.-C. Mbanya ◽  
T. H. Thomas ◽  
R. Taylor ◽  
K. G. M. M. Alberti ◽  
R. Wilkinson

1985 ◽  
Vol 249 (2) ◽  
pp. F299-F307 ◽  
Author(s):  
M. E. Olsen ◽  
J. E. Hall ◽  
J. P. Montani ◽  
A. C. Guyton ◽  
H. G. Langford ◽  
...  

The aim of this study was to determine the role of changes in renal arterial pressure (RAP), renal hemodynamics, and tubular reabsorption in mediating the natriuretic and antinatriuretic actions of angiotensin II (ANG II). In seven anesthetized dogs, endogenous ANG II formation was blocked with captopril, and ANG II was infused intravenously at rates of 5-1,215 ng X kg-1 X min-1 while RAP was either servo-controlled at the preinfusion level or permitted to increase. When RAP was servo-controlled, ANG II infusion at all rates from 5-1,215 ng X kg-1 X min-1 decreased urinary sodium excretion (UNaV) and fractional sodium excretion (FENa) while increasing fractional reabsorption of lithium (FRLi) (an index of proximal tubular fractional sodium reabsorption) and causing no change in calculated distal tubule fractional sodium reabsorption (FRDNa). When RAP was permitted to increase, ANG II infusion rates up to 45 ng X kg-1. min-1 also decreased UNaV and FENa while increasing FRLi and causing no change in FRDNa. However, at 135 ng X kg-1 X min-1 and above, UNaV and FENa increased while FRLi and FRDNa decreased when RAP was allowed to rise, even though renal blood flow and filtration fraction were not substantially different from the values observed when RAP was servo-controlled. Filtered sodium load was slightly higher when RAP was permitted to increase during ANG II infusion compared with when RAP was servo-controlled, although the differences were not statistically significant. Thus, even very large doses of ANG II cause antinatriuresis when RAP is prevented from increasing.(ABSTRACT TRUNCATED AT 250 WORDS)


1989 ◽  
Vol 257 (2) ◽  
pp. F237-F242 ◽  
Author(s):  
Y. Kinoshita ◽  
J. C. Romero ◽  
F. G. Knox

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.


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