Collecting duct is a site of sodium retention in PAN nephrosis: A rationale for amiloride therapy
Collecting duct is a site of sodium retention in PAN nephrosis: A rationale for amiloride therapy
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DOI：
10.1681/asn.v123598
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发表时间：
2001-03-01
影响因子：
13.6
通讯作者：
Doucet, A
中科院分区：
文献类型：
--
作者：
Deschenes, G;Wittner, M;Doucet, A
远端肾单位的显微穿刺研究和显微解剖的集合小管中Na，K-ATP酶活性的测量表明，嘌呤霉素氨基糖苷（PAN）肾病大鼠的肾钠潴留起源于集合管。本研究通过体外微灌注证实了这一假设，并表明阿米洛利能够恢复钠平衡。事实上，从PAN治疗的大鼠中分离的灌注皮质集合管表现出异常高的跨上皮钠重吸收，阿米洛利消除，阿米洛利的体内给药完全防止肾病大鼠尿钠排泄减少和正钠平衡。正如PAN肾病大鼠中Naf潴留的醛固酮独立性所预期的那样，坎利酸钾对醛固酮受体的阻断并没有改变PAN肾病大鼠的尿Na+排泄、Na+平衡或腹水形成。
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 Naf 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.