May 1, 1995Journal of Cardiovascular Pharmacology
Interference of Angiotensin-Converting Enzyme Inhibition with Vasoactive Peptides in the Coronary Circulation of Dogs
Key result
Captopril potentiates neurotensin-induced coronary blood flow increases to ~40% without affecting ET-1 or NPY.
- P<0.01
Why the study?
The coronary effects of ACE inhibitors and their mechanisms of action were not well understood, including potential interference with hormone systems other than the renin-angiotensin system.
Does captopril modulate the coronary effects of neurotensin, neuropeptide Y, and endothelin-1 in anesthetized dogs?
Population
Anesthetized, open-chest dogs
Comparison
Pretreatment with captopril vs control
Design
Preclinical animal study
Authors
Discussion
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Implication
Animal data preclude practice change; leaves open whether ACE inhibition modulates neurotensin coronary effects in humans.
Structured PICO
Does captopril modulate the coronary effects of neurotensin, neuropeptide Y, and endothelin-1 in anesthetized dogs?
P
Population
Anesthetized, open-chest dogs used to study the modulation of coronary effects of vasoactive peptides by captopril.
I
Intervention
Captopril (0.25 mg/kg intracoronary injection followed by 0.25 mg/kg/h infusion) prior to administration of neurotensin, neuropeptide Y (NPY), and endothelin-1 (ET-1)
C
Comparator
Before captopril administration and/or control animals
O
Outcome
Coronary blood flow (CBF) and subendocardial segment lengthsurrogate
Main Result
Absolute Event Rate: 40% vs 20%
p-value: p=< 0.01
ACE inhibition with captopril potentiates the coronary vasodilatory effects of neurotensin but does not alter the acute vasoconstrictor effects of ET-1 or NPY in a canine model.
Cite This Study
Bauer et al. (1995) studied this question. Captopril vs. Before captopril / control animals was evaluated on Increase in coronary blood flow induced by neurotensin (p=< 0.01). Captopril potentiated the increase in coronary blood flow induced by neurotensin (40% vs 20% before captopril, p < 0.01) but did not affect the acute vasoconstrictor effects of ET-1 or NPY.