Role of Angiotensin II and Bradykinin on Aortic Collagen Following Converting Enzyme Inhibition in Spontaneously Hypertensive Rats
Key result
ACE inhibition and AT1 receptor antagonism completely prevented aortic collagen accumulation in spontaneously hypertensive rats independently of blood pressure changes.
Why the study?
Does ACE inhibition, with or without bradykinin antagonism, or angiotensin II AT1 receptor antagonism prevent aortic collagen accumulation in spontaneously hypertensive rats?
Population
Four week-old spontaneously hypertensive rats (SHRs) and Wistar-Kyoto (WKY) control rats
Comparison
Quinapril, quinapril with Hoe 140, or CI996… vs Placebo administered for 4 months
Design
Preclinical
Follow-up
4 months
Authors
Discussion
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Implication
ACEI effects on aortic fibrosis in SHRs may involve bradykinin; leaves open mechanism and relevance in human hypertension.
Structured PICO
Does ACE inhibition, with or without bradykinin antagonism, or angiotensin II AT1 receptor antagonism prevent aortic collagen accumulation in spontaneously hypertensive rats?
P
Population
Four week-old spontaneously hypertensive rats treated for 4 months to evaluate the effects of ACE inhibition on aortic fibrosis.
I
Intervention
Quinapril (ACE inhibitor), quinapril with Hoe 140 (bradykinin B2 receptor antagonist), or CI996 (angiotensin II AT1 receptor antagonist) administered for 4 months
C
Comparator
Placebo administered for 4 months
O
Outcome
Aortic collagen accumulationsurrogate
In spontaneously hypertensive rats, ACE inhibitors prevent aortic fibrosis exclusively through angiotensin II AT1 receptor inhibition, independent of blood pressure reduction or bradykinin preservation.
Cite This Study
Bénétos et al. (1997) studied Hypertension. Quinapril, quinapril with Hoe 140, or CI996 vs. Placebo was evaluated on Aortic collagen accumulation. ACE inhibition and AT1 receptor antagonism completely prevented aortic collagen accumulation in spontaneously hypertensive rats independently of blood pressure changes.