scholarly journals Prevention of Pyelonephritis by Water Diuresis: Evidence for the Role of Medullary Hypertonicity in Promoting Renal Infection *

1965 ◽  
Vol 44 (1) ◽  
pp. 73-79 ◽  
Author(s):  
Vincent T. Andriole ◽  
Franklin H. Epstein
Radiology ◽  
1990 ◽  
Vol 174 (1) ◽  
pp. 283-284 ◽  
Author(s):  
R P Gold ◽  
B L McClennan
Keyword(s):  

2001 ◽  
Vol 281 (5) ◽  
pp. F936-F947 ◽  
Author(s):  
Rajash K. Handa ◽  
Shelly E. Handa ◽  
Monica K. S. Elgemark

Receptor autoradiography revealed that angiotensin AT4 receptors were abundantly expressed in normal mammalian (mouse, rat, gerbil, guinea pig, rabbit) and avian (sparrow, chicken, turkey) kidneys and were more extensively distributed than previously reported (including proximal and distal segments of the nephron, interstitium, renal artery, vein, and ureter). Angiotensin AT4 receptors were generally found to be more abundant than angiotensin AT1 receptors in mammalian kidneys, whereas angiotensin AT(1—7) receptors were not detected in either mammalian or avian kidneys. Rats subjected to various chronic treatments were found to preferentially decrease kidney AT4 receptor density (furosemide, puromycin aminonucleoside, nitro-l-arginine methyl ester), decrease kidney AT1 receptor density (bilateral ureteral obstruction), or increase kidney AT1 receptor distribution in the inner medulla (water diuresis). These results indicate that the AT4 receptor can be expressed in numerous cell types within the normal kidney of several species. Furthermore, several models of renal dysfunction and injury have been identified that selectively alter kidney AT4 density and may potentially aid in elucidating the role of this novel angiotensin receptor system in renal function.


Radiology ◽  
1989 ◽  
Vol 173 (2) ◽  
pp. 574-575 ◽  
Author(s):  
R B Jeffrey
Keyword(s):  

1981 ◽  
Vol 241 (3) ◽  
pp. F231-F237 ◽  
Author(s):  
J. S. Stoff ◽  
R. M. Rosa ◽  
P. Silva ◽  
F. H. Epstein

The mechanisms by which endogenous renal prostaglandins regulate water excretion were investigated in these studies. Inhibition of prostaglandin synthesis slowed water diuresis in water-loaded unanesthetized Sprague-Dawley rats and in Brattleboro rats with hereditary diabetes insipidus owing to absence of endogenous vasopressin. In both strains, treatment with indomethacin or meclofenamate increased the osmolality of the renal papilla by raising sodium and urea content, and also increased the osmolality of the urine. Endogenous creatinine clearance and solute excretion were unchanged. The data are consistent with an effect of prostaglandins on solute transport by renal tubules and demonstrate that endogenous prostaglandins influence water excretion by a mechanism independent of the presence of antidiuretic hormone.


1982 ◽  
Vol 21 (2) ◽  
pp. 365-370 ◽  
Author(s):  
Rebecca M. Walker ◽  
Robert S. Brown ◽  
Jeffery S. Stoff

1998 ◽  
Vol 274 (6) ◽  
pp. R1619-R1625 ◽  
Author(s):  
Elzbieta Kompanowska-Jezierska ◽  
Claus Emmeluth ◽  
Lisbeth Grove ◽  
Poul Christensen ◽  
Janusz Sadowski ◽  
...  

Renal effects of physiological amounts of vasopressin were studied in conscious dogs during servocontrolled overhydration (2% body wt). During infusion of vasopressin (50 pg ⋅ min−1 ⋅ kg body wt−1), plasma vasopressin concentration increased to 2.30 ± 0.20 pg/ml compared with 0.12 ± 0.03 pg/ml during control (water diuresis). With vasopressin infusion, urine flow was significantly lower (0.30 ± 0.10 ml/min) and sodium excretion (UNaV) was significantly higher (58.0 ± 15.8 μmol/min) than without vasopressin (4.6 ± 0.4 ml/min and 14.4 ± 4.1 μmol/min, respectively). Deamino-[Cys1,d-Arg8]vasopressin, a V2 receptor agonist (4 pg ⋅ min−1 ⋅ kg−1), mimicked the antidiuretic response (0.20 ± 0.03 ml/min) without changing UNaV (9.7 ± 4.4 μmol/min). Indomethacin given during arginine vasopressin (AVP) infusion suppressed prostaglandin E2 excretion, intensified the antidiuresis (0.10 ± 0.02 ml/min), and abolished the natriuresis (13.4 ± 3.7 μmol/min). During AVP infusion, UNaV was highly correlated ( r = 0.85) with prostaglandin E2 excretion. Blood pressure, glomerular filtration rate, plasma atrial natriuretic peptide concentration, and the rate of proximal tubule reabsorption (derived from lithium clearance) were similar in all series. The data indicate that, in the dog, physiological amounts of vasopressin can induce natriuresis, probably through activation of non-V2 receptors and the intrarenal synthesis of prostaglandins.


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