Key result
Subpressor Angiotensin II increases coronary collateral blood flow ~48% in normal rats.
Why the study?
The controversial effects of angiotensin II on coronary collateral growth may be due to its regulation of reactive oxygen species and ROS-dependent signaling.
Does Angiotensin II and AT1R blockade regulate coronary collateral growth in normal and syndrome X rats?
Population
Normal (WKY) and syndrome X (JCR) rats subjected to transient/repetitive ischemia
Comparison
Subpressor and hypertensive doses of angiotensin II and AT1R blockade (candesartan) versus transient/repetitive ischemia alone
Design
Preclinical experimental study
Authors
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Animal findings on Ang II and AT1R blockade in rat collaterals should not change practice; hypothesis-generating for human arteriogenesis.
Does Angiotensin II and AT1R blockade regulate coronary collateral growth in normal and syndrome X rats?
Absolute Event Rate: 1.24% vs 0.84%
Angiotensin II and AT1R blockade regulate coronary collateral growth by modulating reactive oxygen species and redox-sensitive signaling pathways (p38 and Akt).
Reed et al. (2007) studied Coronary collateral growth. Angiotensin II and AT1R blockade (candesartan) vs. Transient/repetitive ischemia alone was evaluated on Collateral-dependent zone (CZ) blood flow (mL/min/g). Subpressor Angiotensin II increased collateral blood flow in normal rats (1.24 vs 0.84 mL/min/g), while AT1R blockade reduced it in normal rats but partially restored it in syndrome X rats.
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