Key result
In rats with aorto-caval fistulas, ramipril attenuated right ventricular hypertrophy by 17% on day 7 and potentiated IGF-I increase, whereas losartan had no effect on hypertrophy or IGF-I.
Why the study?
Does ramipril or losartan reduce cardiac hypertrophy and alter IGF-I expression in rats with aorto-caval fistula-induced volume overload?
Does ramipril or losartan reduce cardiac hypertrophy and alter IGF-I expression in rats with aorto-caval fistula-induced volume overload?
In a rat model of volume overload, ACE inhibition with ramipril, but not ARB with losartan, attenuated cardiac hypertrophy and potentiated IGF-I expression.
Ramipril but not losartan attenuated RV hypertrophy via IGF-I in volume-overloaded rats; leaves open class-specific effects for clinical translation.
The effects of angiotensin converting enzyme inhibition and angiotensin II receptor blockade on the development of cardiac hypertrophy and myocardial insulin-like growth factor I (IGF-I) in volume overload were studied in male Wistar rats with aorto-caval fistulas (ACF). Rats were treated with ramipril (RAM, 3 mg kg(-1) day(-1)) for 4-20 days or losartan (LOS, 10 mg kg(-1) day(-1)) for 2-7 days. Myocardial IGF-I and IGF-I receptor (IGF-I-R) mRNA were determined by solution hybridization. ACF caused hypertrophy of left (LV) and right ventricles (RV). Hypertrophy appeared on day 2 and reached maximal values of +60% in LV and +75% in RV at day 12. Systolic blood pressure was initially reduced 15% but recovered by day 12. RAM abolished the recovery of blood pressure. Furthermore, RAM attenuated RV hypertrophy by 17% on day 7 and on day 20, RV weights were close to values found in controls. Beginning on day 9, RAM reduced LV weight back to control levels in parallel to blood pressure. In contrast, LOS affected neither RV nor LV hypertrophy. RV IGF-I mRNA increased 60-100% on day 7 alone in RV in ACF. RAM potentiated the increase in RV IGF-I to +400% and induced an increase in RV IGF-I-R mRNA on day 7 (+90%) in ACF. LOS did not affect RV IGF-I. Development of cardiac hypertrophy in ACF seemed independent of angiotensin II. RV hypertrophy was associated with activation of IGF-I independent of the renin-angiotensin system. IGF-I was further potentiated when development of hypertrophy was attenuated, possibly indicative of a greater urge for compensational growth in a relatively thinner and more volume-distended chamber.
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WÅHLANDER et al. (1999) studied Aorto-caval fistula-induced cardiac hypertrophy. Ramipril or Losartan vs. Controls (untreated ACF) was evaluated on Development of cardiac hypertrophy and myocardial IGF-I. In rats with aorto-caval fistulas, ramipril attenuated right ventricular hypertrophy by 17% on day 7 and potentiated IGF-I increase, whereas losartan had no effect on hypertrophy or IGF-I.
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