March 1, 2002Journal of Clinical Investigation
Evidence for the importance of angiotensin II type 1 receptor in ischemia-induced angiogenesis
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Key result
AT1a receptor deficiency or pharmacological blockade significantly impaired ischemia-induced angiogenesis and blood flow recovery in mice compared to wild-type controls.
Why the study?
Does AT1a receptor deficiency or blockade impair ischemia-induced angiogenesis in a mouse model of hindlimb ischemia?
Population
Male C57BL/6 wild-type mice and AT1a receptor knockout mice, aged 8-10 weeks, subjected to unilateral…
Comparison
AT1a receptor deficiency or pharmacological AT1… vs Wild-type mice with intact AT1a receptors and no…
Design
Preclinical
Follow-up
35 days
Authors
Discussion
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Implication
AT1a signaling may support ischemia-induced angiogenesis in mice; hypothesis-generating and should not change ARB use in patients.
Structured PICO
Does AT1a receptor deficiency or blockade impair ischemia-induced angiogenesis in a mouse model of hindlimb ischemia?
P
Population
Male AT1a knockout and wild-type mice subjected to unilateral hindlimb ischemia to evaluate the role of the AT1a receptor in angiogenesis.
E
Exposure
AT1a receptor deficiency (knockout) or pharmacological AT1 receptor blockade with TCV-116 (5 mg/kg/d oral).
C
Comparator
Wild-type mice with intact AT1a receptors and no AT1 blockade.
O
Outcome
Ischemia-induced angiogenesis assessed by ischemic/normal hindlimb laser Doppler blood flow ratio, angiographic score, and capillary density up to 35 days post-surgery.surrogate
Main Result
p-value: p=<0.05
The angiotensin II type 1 receptor pathway promotes early ischemia-induced angiogenesis by supporting inflammatory cell infiltration and angiogenic cytokine expression.
Limitations
- The dose of TCV-116 used was higher than the clinical dose.
- In several experimental groups, only LDBF values were measured to assess ischemia-induced angiogenesis.
- Western blot analysis of homogenized tissue extracts does not address the possibility that VEGF expression in skeletal muscles may differ between WT and AT1a-/- mice.
Cite This Study
Sasaki et al. (2002) studied Hindlimb ischemia. AT1a receptor deficiency (knockout) or AT1 receptor blockade vs. Wild-type (WT) mice was evaluated on Ischemic/normal hindlimb blood flow ratio (LDBF ratio) (p=<0.05). AT1a receptor deficiency or pharmacological blockade significantly impaired ischemia-induced angiogenesis and blood flow recovery in mice compared to wild-type controls.
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