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자료유형
학술저널
저자정보
저널정보
대한생화학·분자생물학회 Experimental and Molecular Medicine Experimental and Molecular Medicine 제36권 제3호
발행연도
2004.1
수록면
251 - 258 (8page)

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Hypertension and anemia may be causes of left ventricular hypertrophy (LVH) in uremia but the molecular mechanism is not known. Uremia was nephrectomy. The folowing groups of rats were studied for 6 weks; uremic rats (U) fed ad. lib., control rats (C) pair-fed with U, U rats given hydralazine (10 mg/kg/day) (UH), U rats given erythropoietin (48U/kg/wek, i.p.) (UE). Both diastolic and mean arterial pressures are higher (P< 0.01) in U and UE compared with C whereas both presures in UH were normalized. Hemoglobin in U was lower than in C, and was normalized in UE. U, UH and UE had higher as left ventricular weight/body weight ratios (LV/BW) compared with C (P< 0.01). Compared with U, UH has lower HW/BW and LV/BW (P <0.05) and UE has normal HW/BW but lower LV/BW than U (P < 0.05). To see if the gene expresion in uremic LVH is similar to that described in presure overload LVH in which mRNA levels of angiotensin converting enzyme (ACE), transforming growth factor-β1 (TGF-β1), α- actin were increased, we measured these mRNA levels by Northern analysis. TGF-β1, ACE and α-actin mRNA levels were not changed in all 4 groups. ANF mRNA in U and UE was increased 3 fold over C, and normalized in UH. Treatment of anemia with erythropoietin improved uremic LVH but did not change ANF mRNA; whereas treatment of hypertension with hydralazine normalized ANF mRNA but did not completely corect uremic LVH. Thus, gene expresion in uremic LVH is distinct from that in pressure- overload LVH, sugesting that other unidentified factor(s) might be involved in uremic LVH.

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