集合管是PAN肾病中钠潴留的部位：氨氯地平治疗的理论依据。
Collecting duct is a site of sodium retention in PAN nephrosis: a rationale for amiloride therapy.
作者信息
Deschênes Georges, Wittner Monika, Stefano Antonio DI, Jounier Sylvie, Doucet Alain
机构信息
Service de Néphrologie Pédiatrique, Hôpital Armand-Trousseau Assistance Publique-Hôpitaux de Paris, Paris, France.
Laboratoire de Biologie Intégrée des Cellules Rénales, CNRS URA 1859, Service de Biologie Cellulaire, Commissariat à l'Energie Atomique, Saclay, France.
出版信息
J Am Soc Nephrol. 2001 Mar;12(3):598-601. doi: 10.1681/ASN.V123598.
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.
对远端肾单位的微穿刺研究以及对显微解剖的集合小管中钠钾ATP酶活性的测量表明，嘌呤霉素氨基核苷（PAN）肾病大鼠的肾脏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，并表明氨氯吡咪能够恢复钠平衡。事实上，来自PAN处理大鼠的分离灌注皮质集合管表现出异常高的跨上皮钠重吸收，而氨氯吡咪可消除这种重吸收，并且在肾病大鼠体内给予氨氯吡咪可完全防止尿钠排泄减少和钠正平衡。正如从PAN肾病大鼠钠潴留不依赖醛固酮所预期的那样，坎利酸钾对醛固酮受体的阻断并未改变PAN肾病大鼠的尿钠排泄、钠平衡或腹水形成。
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