کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
9309110 | 1249586 | 2005 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Sodium retention in cirrhotic rats is associated with increased renal abundance of sodium transporter proteins
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کلمات کلیدی
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
بیماریهای کلیوی
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چکیده انگلیسی
The rats manifested marked extracellular fluid volume expansion with massive ascites. Plasma aldosterone levels were markedly elevated. Analysis of immunoblots revealed marked increases in the abundances of both of the major aldosterone-sensitive apical transport proteins of the renal tubule, namely the thiazide-sensitive NaCl cotransporter NCC and the epithelial sodium channel alpha subunit (α-ENaC). These results are consistent with an important role for hyperaldosteronism in the pathogenesis of sodium retention and ascites formation in cirrhosis. In addition, we observed a large decrease in cortical NHE3 abundance (proximal tubule) and a large increase in NKCC2 abundance (thick ascending limb), potentially shifting premacula densa sodium absorption from proximal tubule to loop of Henle (which powers urinary concentration and dilution).
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Kidney International - Volume 67, Issue 2, February 2005, Pages 622-630
Journal: Kidney International - Volume 67, Issue 2, February 2005, Pages 622-630
نویسندگان
Patricia Fernandez-Llama, Shana Ageloff, Guillermo Fernandez-Varo, Josefa Ros, Xiaoyan Wang, Nuria Garra, Cristina Esteva-Font, Jose Ballarin, Pere Barcelo, Vicente Arroyo, John B. Stokes, Mark A. Knepper, Wladimiro Jimenez,