Key result
Inhibition of brain angiotensinogen synthesis in transgenic rats significantly attenuated the increase in systolic blood pressure induced by chronic angiotensin II infusion (29.8 vs 46.3 mm Hg; P<0.005).
Why the study?
Does inhibition of brain angiotensinogen synthesis attenuate angiotensin II-induced hypertension and cardiac hypertrophy in rats?
Population
Transgenic rats with permanent inhibition of brain angiotensinogen synthesis [TGR] and Sprague-Dawley rats
Comparison
7 days of chronic angiotensin II infusion vs Sprague-Dawley rats receiving the same…
Design
Preclinical
Follow-up
7 days
Authors
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Central RAS inhibition attenuates Ang II hypertension in rats; leaves open whether brain-targeted therapies merit human investigation.
Does inhibition of brain angiotensinogen synthesis attenuate angiotensin II-induced hypertension and cardiac hypertrophy in rats?
Absolute Event Rate: 29.8% vs 46.3%
p-value: p=<0.005
Inhibition of brain angiotensinogen synthesis in transgenic rats attenuates angiotensin II-induced hypertension and cardiac hypertrophy, demonstrating that the brain renin-angiotensin system mediates these pathological effects.
Baltatu et al. (2000) studied Angiotensin II-induced hypertension and cardiac hypertrophy. Permanent inhibition of brain angiotensinogen synthesis (TGR(ASrAOGEN) rats) vs. Sprague-Dawley rats (parent strain) was evaluated on Increase in systolic blood pressure induced by 7 days of chronic angiotensin II infusion (p=<0.005). Inhibition of brain angiotensinogen synthesis in transgenic rats significantly attenuated the increase in systolic blood pressure induced by chronic angiotensin II infusion (29.8 vs 46.3 mm Hg; P<0.005).
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