Decreased expression of Na,K-ATPase in the kidneys of rats with two-kidney, one-clip hypertension.
- Author:
Seong Kwon MA
1
;
Yoon Wha OH
;
In Jin KIM
;
Eun Hui BAE
;
Jong Un LEE
;
Soo Wan KIM
Author Information
1. Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea. skimw@chonnam.ac.kr
- Publication Type:Original Article
- Keywords:
Renovascular hypertension;
Na,K-ATPase;
Aldosterone synthase;
Atrial natriuretic peptide
- MeSH:
Adult;
Aldosterone;
Aldosterone Synthase;
Animals;
Atrial Natriuretic Factor;
Blood Pressure;
Down-Regulation;
Humans;
Hypertension;
Hypertension, Renovascular;
Immunoblotting;
Kidney;
Male;
Plasma;
Rats;
Rats, Sprague-Dawley;
Receptors, Mineralocorticoid;
Renin;
Renin-Angiotensin System;
RNA, Messenger;
Sodium
- From:Korean Journal of Medicine
2010;78(4):477-484
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND/AIMS: This study investigated the role of Na,K-ATPase, the local renin-angiotensin-aldosterone system (RAAS), and atrial natriuretic peptide (ANP) system in the pathogenesis of renal tubular dysfunction and hypertension in rats with two-kidney, one-clip (2K1C) hypertension. METHODS: Adult male Sprague-Dawley rats were made 2K1C hypertensive for 4 weeks. The renal expression of Na,K-ATPase was determined by immunoblotting. The mRNA expression of renin, angiotensin-converting enzyme (ACE), aldosterone synthase (CYP11B2), mineralocorticoid receptor (MR), and the ANP system were determined in the kidney using real-time polymerase chain reaction. RESULTS: The blood pressure was increased in the 2K1C rats, compared with controls. The plasma renin activity and serum aldosterone concentrations were increased, as were the urine output and fractional excretion of sodium. The expression of Na,K-ATPase protein was decreased in the clipped kidney, as compared with the control kidney, while it remained unchanged in the contralateral kidney. The mRNA expression of renin, ACE1, CYP11B2, and MR was increased in the clipped kidney, but unchanged in the non-clipped kidney. The mRNA expression of ACE2 did not differ between the groups. The expression of ANP mRNA was increased in both clipped and non-clipped kidneys, as compared with control kidneys. CONCLUSIONS: The enhanced activity of the local RAAS may result in to ischemic tubular injury and the development of hypertension in 2K1C rats. The downregulation of Na,K-ATPase associated with tubular injury in the clipped kidney may account for the impaired tubular sodium reabsorption in 2K1C hypertension.
