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July 24, 2009Arteriosclerosis Thrombosis and Vascular Biology

Impaired Recovery of Blood Flow After Hind-Limb Ischemia in Mice Lacking Guanylyl Cyclase-A, a Receptor for Atrial and Brain Natriuretic Peptides

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Population

Mice with hind-limb ischemia and cultured human endothelial cells.

Comparison

Guanylyl cyclase-A deficiency in vivo; ANP… vs Wild-type mice in vivo; untreated cells in vitro.

Design

Preclinical

Follow-up

28 days

Authors

TTTakeshi TokudomeYokohama City UniversityIKIchiro KishimotoKansai Medical UniversityKYKenichi YamaharaHyogo Medical University

Discussion

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Implication

GC-A signaling may aid post-ischemic repair; hypothesis-generating in mice and should not yet change practice.

Structured PICO

P
Population
Mice with hind-limb ischemia (GC-A-deficient mice, n=10, and wild-type mice, n=10) and cultured human endothelial cells.
I
Intervention
Guanylyl cyclase-A (GC-A) deficiency (genetic knockout) in vivo; ANP treatment in vitro.
C
Comparator
Wild-type (WT) mice in vivo; untreated cells in vitro.
O
Outcome
Recovery of blood flow, tissue necrosis/amputation, and capillary density in the ischemic limb.surrogate

Endogenous ANP and BNP signaling via GC-A plays a critical role in reparative vascular remodeling and blood flow recovery following ischemia.

Cite This Study

Tokudome et al. (2009) studied this question.

synapsesocial.com/papers/6a9136fab18f518eae4638fdhttps://doi.org/10.1161/atvbaha.109.187526
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