Effect of Adrenalectomy on Spontaneous and Induced Proteinuria in the Rat.

Addis, T.; Marmorston, Jessie; Goodman, Harold S.; Sellers, Alvin L.; Smith, Margaret M.

doi:10.3181/00379727-74-17803

Cited by 39 publications

(24 citation statements)

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“…1). It has been demonstrated previously, that the intraperitoneal injection of renin fails to increase proteinuria in the salt-maintained adrenalectomized rat (9,10). Since intravenous renin elicits a normal pressor response in the adrenalectomized rat, a study was made of the proteinuric effects of intravenous renin in normal and adrenalectomized animals.…”

Section: Resultsmentioning

confidence: 89%

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Studies on the Mechanism of Experimental Proteinuria

Sellers

Smith

Marmorston

et al. 1952

Journal of Experimental Medicine

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Proteinuria may be produced in the experimental animal in a variety of ways. One of the simplest and most convenient methods is injection of the kidney enzyme, renin.Picketing and Prinzmetal (1) were the first to notice that proteinuria was increased following renin administration to the rabbit. Brandt and Gruhn (2) confirmed this finding, and by studying the simultaneous excretion of injected hemoglobin, concluded that renin does not significantly alter the glomerular permeability, but rather increases proteinuria by diminishing tubular reabsorption of protein from the glomerular filtrate. Shortly after this, Addis, Barrett, Boyd, and Ureen (3) discovered that renin produced an intense, though transient, proteinuria in the rat. Since inactivation of renin, with respect to its pressor effect, led to a loss of its capacity to induce proteinuria, and since repeated injections of renin, at suitable intervals, led to a diminution in the proteinuric as well as the pressor property of renin, these workers concluded that this form of proteinuria is dependent on the pressor action of renin. Rather and Addis (4) reported that the athrocytosis of simultaneously administered hemoglobin or bovine albumin by the cells lining the proximal convoluted tubule is not inhibited by renin, and stated that Brandt and Gruhn's hypothesis, that renin inhibits the tubular reabsorption of protein, is not supported by their experiments. More recently, Lippman, Ureen, and Oliver (5) have restudied the effect of renin on the excretion of injected hemoglobin. From a combination of morphological and functional data these workers conclude that renin causes an increase in glomerular permeability to hemoglobin and decreases the tubular reabsorption of this substance. Hence, conflicting views are expressed concerning the mechanism whereby renin produces an increased excretion of protein in the urine.

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Section: Resultsmentioning

confidence: 89%

“…In the hour following the intraperitoneal injection of 4 units of renin, an average of 31.7 mg. of protein is excreted (9). It has been shown that the peak of proteinuria following the intraperitoneal injection of renin occurs during the 1st hour, and that animals excrete very little (3).…”

Section: Resultsmentioning

confidence: 99%

Studies on the Mechanism of Experimental Proteinuria

Sellers

Smith

Marmorston

et al. 1952

Journal of Experimental Medicine

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“…However, in the hour following the intraperitoneal injection of 4 Goldblatt dog units of hog renin the excretion of protein increased to an average value of 31.7 rag. (5). Gilson (6) fraetionated the urinary protein of normal rats with ammonium sulfate, and found approximately equal quantities of albumin and globulin.…”

Section: (From the Institute For Medical Research Cedars Of Lebanon mentioning

confidence: 99%

An Electrophoretic Study of Urinary Protein in the Rat

Sellers

Roberts

Rask

et al. 1952

Journal of Experimental Medicine

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The administration of renin to the rabbit or the rat causes marked changes in the composition of the urine (1-3). The adult female rat normally excretes 0.1 to 0.2 mg. of protein in its urine per hour, while the adult male rat excretes from three to five times this amount (4). However, in the hour following the intraperitoneal injection of 4 Goldblatt dog units of hog renin the excretion of protein increased to an average value of 31.7 rag. (5). Gilson (6) fraetionated the urinary protein of normal rats with ammonium sulfate, and found approximately equal quantities of albumin and globulin. Wicks (7) found traces of albumin and globulin in normal mouse urine, but concluded that the greater portion of the urinary protein consisted of nucleoprotein. Parfentjiv and Perlzweig (8) reported that the protein present in the urine of normal male mice was a chondromucoid substance. The nature of the protein excreted in the urine following renin administration is not known. The present report describes an electrophoretic study of normal urinary proteins in the rat, and of the proreins appearing in the urine following the administration of renin. MethodsAdult male and female albino rats of the Slonaker-Addis strain weighing from 150 to 200 gm. were used in these experiments. These animals were maintained on a diet containing 17 per cent protein and adequate quantities of all of the known essential food factors. Preparation of Normal Rat UrinaryProteins.--Groups of fifteen animals of the same sex were taken from the colony at 4:00 p.m. and placed in individual metabolism cages. The voided urine was collected during the ensuing 17 hours. The technique used for the collection of uncontaminated urine has been described elsewhere (2).

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“…Other examples of conflicting opinions about the sensitivity of rat strains to the development of CPN exist, due to the fact that comparison of CPN progression and severity between rat strains is difficult, because of the profound effect of a number of environmental variables upon the genetic background of the rat strain or stock in question. The disease is more severe in male than female rats (6, 12, 21) and can be abbrogated by castration or enhanced with testosterone (21), thyroxin and adrenal hormones (22). Dietary protein, carbohydrates and sodium excess (3-5, 10-12) or amino acid toxicity (4, 5) also influence the disease.…”

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confidence: 99%

Chronic Progressive Nephropathy in Aging Rats

Barthold

1979

Toxicol Pathol

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Chronic progressive nephropathy (CPN) i s a commonly encountered lesion i n aging laboratory rats. CPN has been given a variety of names, based upon i t s complex nature. It is a lesion that occurs primarily in albino strains and is influenced not only by genetics but also by sex, age, hormones, diet, and microflora, among other factors. Affected kidneys are enlarged, pale and finely indented. The lesion begins with progressive thickening of glomerular, Bowman's capsular and proximal tubular basement membranes. Mesangial matrix increases with deposition of IgM and, to a lesser extent, other serum components. Tubular atrophy and degenerative changes occur as the lesion progresses. The disease is manifested by increasingly non-selective proteinuria, consisting mainly of albumin. Serum chemical changes include elevations in a globulins and cholesterol and a decrease in albumin. Creatinine and urea remain unchanged until late in the course of CPN. Renal secondary hyperparathyroidism may occasionally be seen.

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Effect of Adrenalectomy on Spontaneous and Induced Proteinuria in the Rat.

Cited by 39 publications

References 0 publications

Studies on the Mechanism of Experimental Proteinuria

Studies on the Mechanism of Experimental Proteinuria

An Electrophoretic Study of Urinary Protein in the Rat

Chronic Progressive Nephropathy in Aging Rats

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