Abstract
Aims: To determine whether the renal regulation of aquaporin (AQP) water channels and sodium transporters are altered in 2-kidney, 1-clip (2K1C) hypertension. Methods: 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. Results: 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 α1-subunit, type 3 Na<sup>+</sup>/H<sup>+</sup> exchanger, Na-K-2Cl cotransporter and epithelial sodium channels were decreased in the clipped kidney, while remaining unchanged in the non-clipped kidney. Conclusion: 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.
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