March 1, 2002Open Access

Evidence for the importance of angiotensin II type 1 receptor in ischemia-induced angiogenesis

Q: What is the clinical evidence from this study?

Study design: Other. Population: Hindlimb ischemia. Intervention: AT1a receptor deficiency or TCV-116 (AT1 receptor blocker) vs. Wild-type mice. Primary outcome: Ischemic/normal hindlimb blood flow ratio (p=<0.05).

Key Result

Angiotensin II type 1a receptor deficiency or pharmacological blockade significantly impaired ischemia-induced angiogenesis and blood flow recovery in a mouse model of hindlimb ischemia.

PICO

Population

Hindlimb ischemia

Intervention / Comparator

AT1a receptor deficiency or TCV-116 (AT1 receptor blocker) vs Wild-type mice (TCV-116 5 mg/kg/d)

Primary Outcome

Ischemic/normal hindlimb blood flow ratio, p=<0.05

Main Result

p-value: p=<0.05

Limitations

The dose of TCV-116 was higher than the clinical dose.
In several experimental groups, only laser Doppler blood flow values were measured to assess ischemia-induced angiogenesis.
Western blot analysis of homogenized tissue extracts does not address potential differences in skeletal muscle VEGF expression.

Abstract

stem cells with a targeted

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Cite This Study

Sasaki et al. (Fri,) conducted a other in Hindlimb ischemia. AT1a receptor deficiency or TCV-116 (AT1 receptor blocker) vs. Wild-type mice was evaluated on Ischemic/normal hindlimb blood flow ratio (p=<0.05). Angiotensin II type 1a receptor deficiency or pharmacological blockade significantly impaired ischemia-induced angiogenesis and blood flow recovery in a mouse model of hindlimb ischemia.

synapsesocial.com/papers/6a1d9c0ccc9f7df1b705b22a https://doi.org/https://doi.org/10.1172/jci0213055