Na(+)-K(+)-ATPase activity: role in the impaired sodium excretion of experimental nephrosis in rats.
Using the model of adriamycin-induced nephrotic syndrome in rats, we studied the relationship between urine electrolyte excretion rates and proteinuria and determined the activity of Na(+)-K(+)-ATPase in the renal tissue of nephrotic rats. No relationship was found between the increased sodium reabsorption and proteinuria. But the impaired salt excretion was inversely related to the increase of Na(+)-K(+)-ATPase activity in the renal inner medulla. It is proposed that direct effect of adriamycin on renal tubule cells is the primary events, that the increased Na(+)-ATPase activity on basolateral membrane of renal tubule cells be an intrarenal factor which mediates the action of retention of salt by the kidney and that inner medullary collecting ducts might be one of the sites of the sodium retention in nephrotic rats.
Lu
S G
SG
Pediatric Nephrology Center, Nanjing Medical University.
Jiang
X Y
XY
Hu
M C
MC
Guo
M
M
D000419:Albuminuria / Q000201:enzymology; D000818:Animals; D004317:Doxorubicin; D008297:Male; D009404:Nephrotic Syndrome / Q000139:chemically induced / Q000201:enzymology* / Q000652:urine; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000652:urine*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D004317:Doxorubicin; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase