Abstract |
Micropuncture studies of the distal nephron and measurements of Na,K- ATPase activity in microdissected collecting tubules have suggested that renal retention of sodium in puromycin aminonucleoside (PAN) nephrotic rats originates in the collecting duct. The present study demonstrated this hypothesis by in vitro microperfusion and showed that amiloride was able to restore sodium balance. Indeed, isolated perfused cortical collecting ducts from PAN-treated rats exhibited an abnormally high transepithelial sodium reabsorption that was abolished by amiloride, and in vivo administration of amiloride fully prevented decreased urinary sodium excretion and positive sodium balance in nephrotic rats. As expected from the aldosterone independence of Na(+) retention in PAN nephrotic rats, blockade of aldosterone receptor by potassium canrenoate did not alter urinary Na(+) excretion, Na(+) balance, or ascites formation in PAN nephrotic rats.
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Authors | Georges Deschênes, Monika Wittner, Antonio DI Stefano, Sylvie Jounier, Alain Doucet |
Journal | Journal of the American Society of Nephrology : JASN
(J Am Soc Nephrol)
Vol. 12
Issue 3
Pg. 598-601
(Mar 2001)
ISSN: 1046-6673 [Print] United States |
PMID | 11181809
(Publication Type: Journal Article)
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Chemical References |
- Mineralocorticoid Receptor Antagonists
- Sodium Channel Blockers
- Puromycin Aminonucleoside
- Amiloride
- Canrenoic Acid
- Sodium
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Topics |
- Amiloride
(therapeutic use)
- Animals
- Canrenoic Acid
(therapeutic use)
- In Vitro Techniques
- Kidney Tubules, Collecting
(drug effects, metabolism)
- Male
- Mineralocorticoid Receptor Antagonists
(therapeutic use)
- Natriuresis
(drug effects)
- Nephrotic Syndrome
(chemically induced, drug therapy, metabolism)
- Perfusion
- Puromycin Aminonucleoside
(toxicity)
- Rats
- Rats, Sprague-Dawley
- Sodium
(metabolism)
- Sodium Channel Blockers
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