Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
Kidney Blood Press Res. 2009;32(6):411-20. doi: 10.1159/000264232. Epub 2009 Dec 3.
To determine whether the renal regulation of aquaporin (AQP) water channels and sodium transporters are altered in 2-kidney, 1-clip (2K1C) hypertension.
Male Sprague-Dawley rats were used. They were made 2K1C hypertensive for 1 week. The renal expression of AQPs and sodium transporters was determined by semiquantitative immunoblotting and immunohistochemistry. The activity of adenylyl cyclase was measured by stimulated generation of cAMP.
Systolic blood pressure was increased in 2K1C rats. Experimental rats revealed impaired urinary concentration in association with increased urine volume. Urinary sodium excretion also increased. The expression of AQP1-3 was decreased in the clipped kidney compared with the control kidney, whereas it was unchanged in the non-clipped kidney. The adenylyl cyclase activity provoked by arginine vasopressin, sodium fluoride or forskolin was blunted in the clipped kidney, but remained unaltered in the contralateral kidney. The expressions of the Na,K-ATPase alpha1-subunit, type 3 Na(+)/H(+) exchanger, Na-K-2Cl cotransporter and epithelial sodium channels were decreased in the clipped kidney, while remaining unchanged in the non-clipped kidney.
The downregulation of AQPs and major sodium transporters/channels in the clipped kidney may play a role in the urinary concentration defect and impaired sodium reabsorption in 2K1C hypertension.
确定 2 肾 1 夹(2K1C)高血压是否改变了水通道蛋白(AQP)和钠转运体的肾脏调节。
雄性 Sprague-Dawley 大鼠用于实验。使大鼠形成 2K1C 高血压 1 周。通过半定量免疫印迹和免疫组织化学测定 AQP 和钠转运体的肾表达。通过刺激 cAMP 的产生来测量腺苷酸环化酶的活性。
2K1C 大鼠的收缩压升高。实验大鼠表现出尿浓缩功能受损,同时伴有尿量增加。尿钠排泄也增加。与对照侧肾脏相比,夹闭侧肾脏的 AQP1-3 表达减少,而非夹闭侧肾脏的 AQP1-3 表达不变。血管加压素、氟化钠或福司可林刺激引起的腺苷酸环化酶活性在夹闭侧肾脏减弱,但在对侧肾脏不变。Na,K-ATPase alpha1-亚单位、型 3 Na+/H+ 交换器、Na-K-2Cl 共转运体和上皮钠通道的表达在夹闭侧肾脏减少,而在非夹闭侧肾脏不变。
夹闭侧肾脏中 AQP 和主要钠转运体/通道的下调可能在 2K1C 高血压中的尿浓缩缺陷和钠重吸收受损中起作用。