Key result
Perindopril and losartan lower perfusion pressures but fail to prevent LV growth or subsequent hypertension.
Why the study?
The role of angiotensin II in the development of prehypertensive vascular hypertrophy and its impact on hypertension progression in spontaneously hypertensive rats was unclear.
Does early treatment with perindopril or losartan prevent prehypertensive vascular hypertrophy and subsequent hypertension in spontaneously hypertensive rats?
Does early treatment with perindopril or losartan prevent prehypertensive vascular hypertrophy and subsequent hypertension in spontaneously hypertensive rats?
Early inhibition of the renin-angiotensin system in spontaneously hypertensive rats alters hindquarter vascular reactivity but does not prevent cardiac hypertrophy or the long-term development of hypertension.
Answers are grounded in this paper and cite their sources.
Early RAS blockade does not prevent hypertension in SHR; leaves open translation to human prehypertension.
OBJECTIVE: To examine the role played by angiotensin II (AII) in the development of prehypertensive vascular hypertrophy in the spontaneously hypertensive rat (SHR) and to determine whether normalization of prehypertensive vascular hypertrophy attenuates the development of hypertension. DESIGN: Male SHR and Wistar-Kyoto (WKY) rats were treated from age 10 days until age 6 weeks with perindopril, an angiotensin converting enzyme (ACE) inhibitor, or with losartan, a type 1 AII receptor antagonist. METHODS: At termination of treatment, or 8 weeks after cessation of treatment, vascular growth was assessed by measurement of hindquarter resistance properties and of the medial cross-sectional area of first-order mesenteric arteries. The growth of the heart was assessed by measurement of the left ventricle:body weight ratio. RESULTS: Perindopril and losartan treatment of SHR and WKY rats led to a heterogeneous response in the vasculature, resulting in a reduction in perfusion pressures at maximum dilatation and constriction in the hindquarter vasculature but no significant change in medial cross-sectional area of small mesenteric arteries. Neither perindopril nor losartan treatment affected the growth of the left ventricle in the SHR. After the cessation of treatment the development of hypertension in the losartan- and perindopril-treated SHR did not differ from that in controls. CONCLUSION: These results suggest that AII, acting via angiotensin type 1 receptors, plays an important role in determining the early post-natal reactivity of the hindquarter vasculature but not the medial cross-sectional area of the mesenteric vasculature, which implies that different growth regulatory mechanisms are operating in the two vascular beds. The lack of effect in some vascular beds, together with the lack of effect on the heart, may account for the absence of a persistent effect on the blood pressure.
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Black et al. (1997) studied Prehypertensive vascular hypertrophy and hypertension. Perindopril or losartan vs. Control was evaluated on Vascular growth (hindquarter resistance properties and medial cross-sectional area of mesenteric arteries) and heart growth. Perindopril and losartan reduced perfusion pressures in the hindquarter vasculature but did not affect mesenteric artery area, left ventricular growth, or subsequent development of hypertension.
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