Key result
In dogs with acute myocardial ischemia, ACE inhibition with benazeprilat increased plasma renin activity and angiotensin I, while angiotensin II and angiotensin-(1-7) did not change.
Why the study?
Does ACE inhibition with benazeprilat alter the profile of angiotensin peptides during acute myocardial ischemia in dogs?
Population
Dogs subjected to acute myocardial ischemia produced by occlusion of the left anterior descending coronary…
Comparison
Angiotensin converting enzyme inhibition with… vs Untreated state (before blockade)
Design
Preclinical
Authors
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Supports alternate angiotensin pathways in ischemia; hypothesis-generating and should not alter clinical practice.
Does ACE inhibition with benazeprilat alter the profile of angiotensin peptides during acute myocardial ischemia in dogs?
The study demonstrates that angiotensin peptides can be formed endogenously by enzymatic pathways alternate to converting enzyme during acute myocardial ischemia.
Santos et al. (1990) studied Acute myocardial ischemia. Benazeprilat (CGS-14,831) vs. Untreated animals (baseline) was evaluated on Profile of angiotensin peptides (renin activity, angiotensin I, II, 1-7) in the periphery and across the circulation of the heart. In dogs with acute myocardial ischemia, ACE inhibition with benazeprilat increased plasma renin activity and angiotensin I, while angiotensin II and angiotensin-(1-7) did not change.
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