| Decreased expression of Na,K-ATPase in the kidney in rats with two-kidney, one clip hypertension |
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Seong Kwon Ma, Yoon Wha Oh, In Jin Kim, M.S., Eun Hui Bae, Jong Un Lee, Ki Chul Choi, Soo Wan Kim |
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경희대학교 의과대학 순환기내과학교실 |
| 신혈관성 고혈압 흰쥐 신장에서 Na,K-ATPase 단백 발현 감소 |
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마성권&#;오윤화&#;김인진&#;배은희&#;이종은&#;최기철&#;김수완, Yoon Wha Oh, In Jin Kim, M.S., Eun Hui Bae, Jong Un Lee, Ki Chul Choi, Soo Wan Kim |
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| Abstract |
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Background : The present study was aimed to investigate whether the regulation of Na,K-ATPase in the kidney is altered in two-kidney, one clip (2K1C) hypertension.
Methods : Adult male Sprague-Dawley rats were made 2K1C hypertensive for 4 weeks. The protein expression of Na,K-ATPase was determined in the kidneys by semiquantitative immunoblotting. The mRNA expressions of local renin-angiotensin-aldosterone system (RAAS), aldosterone synthase (CYP11B2) and natriuretic peptide system were determined in the clipped and contralateral kidneys by real-time polymerase chain reaction.
Results : The blood pressure was increased in 2K1C rats compared with controls. Plasma renin activity and serum aldosterone concentrations were increased. Urine output and fractional excretion of sodium were increased. The protein expression of α1 subunit of Na,K-ATPase was decreased in the clipped kidney compared to control kidney, while remained unchanged in the contralateral kidney. The mRNA expressions of renin, angiotensin converting enzyme 1 (ACE1), CYP11B2, mineralocorticoid receptor were increased in the clipped kidney, while unchanged in the non-clipped kidney. The mRNA expression of ACE2 did not differ among the groups. The expression of atrial natriuretic peptide (ANP) mRNA was increased both clipped and non-clipped kidneys compared to control kidney.
Conclusions : The enhanced activities of local RAAS may be attributed to ischemic tubular injury as well as development of hypertension in 2K1C rats. The down-regulation of Na,K-ATPase associated with tubular injury in the clipped kidney may in part account for the impaired tubular sodium reabsorption in 2K1C hypertension. |
| Key Words:
Renovascular hypertension, Na,K-ATPase, Aldosterone synthase, Atrial natriuretic peptide |
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