pituitrin and Kidney-Papillary-Necrosis

pituitrin has been researched along with Kidney-Papillary-Necrosis* in 4 studies

Trials

1 trial(s) available for pituitrin and Kidney-Papillary-Necrosis

ArticleYear
Effect of vasopressin on the reabsorption of phenacetin and its metabolites from the tubular fluid in man.
    Clinical science, 1972, Volume: 43, Issue:5

    Topics: Acetaminophen; Aniline Compounds; Creatinine; Diuresis; Humans; Kidney Papillary Necrosis; Kidney Tubules; Phenacetin; Urea; Vasopressins

1972

Other Studies

3 other study(ies) available for pituitrin and Kidney-Papillary-Necrosis

ArticleYear
Role of urinary concentrating ability in the generation of toxic papillary necrosis.
    Kidney international, 1983, Volume: 23, Issue:5

    We studied the pathogenesis of chemically induced papillary necrosis in six groups of rats. Papillary necrosis was produced by a single injection of 2-bromoethylamine hydrobromide (BEA), 50 mg, i.v.; the animals were followed for 7 to 10 days after the administration of the compound. Following BEA, heterozygous Brattleboro rats developed all the functional and morphologic lesions of papillary necrosis that we previously described in Sprague-Dawley rats. They were unable to maintain sodium balance when dietary sodium was withdrawn. Homozygous Brattleboro rats, on the other hand, developed none of the manifestations of papillary necrosis (that is, animals with central diabetes insipidus were protected completely from the nephrotoxic effects of BEA). They adapted normally to a zero sodium diet. Chronic administration of vasopressin to homozygous Brattleboro rats fully restored the toxic effects of BEA. Lowering urinary concentrating ability by inducing a water diuresis in Sprague-Dawley rats completely protected against BEA-induced papillary necrosis. Decreasing papillary solute concentration by furosemide or increasing urine flow after abrupt withdrawal of vasopressin to homozygous Brattleboro rats did not protect against BEA-induced papillary necrosis. We conclude that the combination, but not either alone, of increased urine flow and decreased papillary solute concentration protects against the development of BEA-induced papillary necrosis.

    Topics: Animals; Diuresis; Ethylamines; Heterozygote; Homozygote; Kidney Concentrating Ability; Kidney Papillary Necrosis; Male; Rats; Rats, Brattleboro; Rats, Inbred Strains; Vasopressins

1983
Factors influencing the severity and progress of ethylenimine-induced papillary necrosis.
    The Journal of pathology, 1982, Volume: 137, Issue:4

    The severity of the renal papillary necrosis produced in rats by ethylenimine is dependent both on dose and urinary concentration within the medulla. When this is reduced by diuresis, the severity of the lesion is effectively reduced. Increasing urinary concentration has a reverse effect, but of less magnitude. When the concentrating power of the renal medulla is impaired by a single dose of ethylenimine, insufficient to cause necrosis of the whole papilla, further doses of ethylenimine do not cause progressive damage to the papilla.

    Topics: Ammonium Chloride; Animals; Arginine Vasopressin; Aziridines; Azirines; Bicarbonates; Diuresis; Female; Kidney Medulla; Kidney Papillary Necrosis; Rats; Vasopressins; Water Deprivation

1982
Experimental renal papillary necrosis. Effects of diuresis and antidiuresis.
    Archives of pathology, 1968, Volume: 85, Issue:4

    Topics: Animals; Bromides; Dehydration; Diuresis; Ethylamines; Injections, Subcutaneous; Kidney; Kidney Concentrating Ability; Kidney Papillary Necrosis; Osmosis; Rats; Renal Veins; Vasopressins

1968