Natriuresis-induced protection in acute myohemoglobinuric renal failure without renal cortical renin content depletion in the rat.
The interrelationships of renal cortical renin content RCRC, sodium chloride excreting and the severity of renal failure were studied in the glycerol-induced acute myohemoglobinuric renal failure model in the rat. Protocols were designed to increase sodium chloride excretion without necessarily resulting in RCRC depletion. Our data fail to demonstrate a relationship between RCRC and severity of renal failure, but they demonstrate an excellent inverse correlation between the sodium chloride excretion of the animals in the 24 h prior to glycerol administration and the severity of resulitng renal failure. The protection of long-term saline-drinking animals should properly be ascribed to the associated natriuresis which develops much before RCRC depletion during the time course of saline drinking. The exact mechanism by which natriuresis exerts its protective effect needs further elucidation, but our data argue against a major role for RCRC in the pathogenesis of acute experimental renal failure.
D058186:Acute Kidney Injury / Q000139:chemically induced / Q000517:prevention & control*; D000818:Animals; D001806:Blood Urea Nitrogen; D002712:Chlorides / Q000652:urine; D004195:Disease Models, Animal; D005260:Female; D005990:Glycerol; D006456:Hemoglobinuria / Q000139:chemically induced / Q000517:prevention & control*; D007672:Kidney Cortex / Q000378:metabolism*; D009212:Myoglobinuria / Q000139:chemically induced / Q000517:prevention & control*; D009318:Natriuresis; D011188:Potassium / Q000652:urine; D051381:Rats; D012083:Renin / Q000378:metabolism*; D012965:Sodium Chloride / Q000652:urine
D002712:Chlorides; D012965:Sodium Chloride; D012083:Renin; D005990:Glycerol; D011188:Potassium