Kreutz R, Fernandez-Alfonso M S, Ganten D, Paul M
Max Delbrück Centre (MDC) for Molecular Medicine, Berlin, Germany.
Clin Exp Hypertens. 1996 Jan;18(1):101-11. doi: 10.3109/10641969609082610.
The aim of this study was to investigate the effect of prophylactic treatment with the angiotensin type 1 (AT1) receptor antagonist losartan on right ventricular hypertrophy and cardiac angiotensin 1-converting enzyme (ACE) activity in a rat model of monocrotaline-induced pulmonary hypertension. Losartan failed to prevent either pulmonary hypertension or right ventricular hypertrophy. Right ventricular ACE in untreated pulmonary hypertensive rats did not differ from control rats. Losartan treatment in pulmonary hypertensive rats caused a significant 2-fold increase of ACE activity in the hypertrophied right (p < 0.005) but not in the left ventricle. Thus, cardiac ACE activity is not stimulated in rats with monocrotaline-induced right ventricular hypertrophy. Prophylactic losartan treatment in this model of progressive pulmonary hypertension failed to prevent or reduce the increase in ventricular afterload. The relevance of the increase in right ventricular ACE activity during pulmonary hypertension after losartan treatment is unknown and needs to be evaluated in further studies.
本研究的目的是在一种由野百合碱诱导的肺动脉高压大鼠模型中,研究使用血管紧张素1型(AT1)受体拮抗剂氯沙坦进行预防性治疗对右心室肥厚和心脏血管紧张素1转换酶(ACE)活性的影响。氯沙坦未能预防肺动脉高压或右心室肥厚。未经治疗的肺动脉高压大鼠的右心室ACE与对照大鼠无差异。氯沙坦治疗肺动脉高压大鼠导致肥厚的右心室(p < 0.005)而非左心室的ACE活性显著增加2倍。因此,在野百合碱诱导的右心室肥厚大鼠中,心脏ACE活性未受到刺激。在这种进行性肺动脉高压模型中,预防性使用氯沙坦治疗未能预防或减少心室后负荷的增加。氯沙坦治疗后肺动脉高压期间右心室ACE活性增加的相关性尚不清楚,需要在进一步研究中进行评估。