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R L Baranowski

Publications and source records attributed to R L Baranowski.

22 records · Page 2Linked to original sources
PubMed1977

Relationship between mineralocorticoids and renal Na+-K+-ATPase: sodium reabsorption.

To evaluate the mechanism responsible for the effect of deoxycorticosterone acetate (DOCA) on renal Na+-K+-ATPase, we compared the relative contribution of this hormone and of increased absolute sodium reabsorption (TNa) to the restoration of the enzyme in kidneys of adrenalectomized rats. In study A, adrenalectomized animals maintained on a salt-free diet received 5 mg/kg per day DOCA i.m., while sham-operated and untreated adrenalectomized rats receiving the same diet served as controls. Absolute TNa and Na+-K+-ATPase specific activity in the cortex and outer medulla of DOCA-treated rats were similar to those measured in untreated adrenalectomized animals, but were significantly lower than in sham-operated controls. In study B, the adrenalectomized rats did not receive DOCA but were fed a high salt diet and received isotonic saline, 50 ml/kg per day s.c. Absolute TNa and cortical and medullary Na+-K+-ATPase specific activity were significantly higher in the salt-loaded group than in both adrenalectomized and sham-operated rats deprived of salt. These results suggest that absolute sodium reabsorption is a major determinant of renal Na+-K+-ATPase activity, and that the effect of DOCA on this enzyme is secondary to its stimulation of absolute tubular sodium transport.

Adenosine Triphosphatases↗
PubMed1975

The effect of 1-sarcosine, 8-leucyl angiotensin II on glycerol-induced acute renal failure.

Several studies have suggested that increased activity of the renin-angiotensin system plays an important role in the pathogenesis of acute renal failure. An analog of angiotensin II, 1-sarcosine, 8-leucyl angiotensin II (AIIA), a potent antagonist of the pressor response of angiotensin II (AII), was injected (16 mug/200 gm) or infused (1.5 mug/200 gm/min) intravenously into glycerol treated (8 ml/kg) rats to evaluate the involvement of the renin-angiotensin system as a mediator in the pathogenesis of acute renal failure. Dehydrated animals, whether untreated, given AIIA, or saline became progressively azotemic and died with 72 hours after glycerol administration. Plasma renin activity, as measured by radioimmunoassay, decreased below dehydrated control levels at one hour after glycerol administration (7.45 ng/ml/hr +/- 1.29 (SE) to 3.24 +/- 0.64), and progressively increased to a maximum 9.9 +/- 0.98) at 17 hours; there was no difference between dehydrated control levels and those obtained 24 and 48 hours after glycerol. Nondehydrated glycerol treated rats were studied as above. These animals developed a non-lethal form of acute renal failure, the severity of which was also unaffected by AIIA administration. These observations indicate that AIIA neither prevents nor alters the development of glycerol induced acute renal failure.

Acute Kidney Injury↗