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Contribution of prostacyclin regulation in the vascular tone of angiopoietin like‐2 deficient mice
Author(s) -
Yu Carol,
Farhat Nada,
Thorin Eric
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.866.22
Subject(s) - prostacyclin , medicine , endocrinology , phenylephrine , vasodilation , nitric oxide , femoral artery , endothelium , chemistry , acetylcholine , blood pressure
Vascular tone, in response to acetylcholine (ACh), is controlled by various endothelium‐derived relaxing factors, which include nitric oxide (NO), prostacyclin, and endothelium‐derived hyperpolarizing factor. In turn, contribution of each factor may be influenced by pathologies. As such, in the insulin resistant state, NO production is impaired. Angiopoietin like‐2 (Angptl2), a member of the angiopoietin‐like protein family, was shown to cause insulin resistance related to obesity (Tabata, 2009). Objective An Angptl2 knock‐down (KD) mouse model was generated to study the role of Angptl2 in endothelial function in the femoral artery. Results Femoral arteries of 4‐month old Angptl2 KD and wild‐type (WT) mice showed that NO was responsible for the sensitivity of ACh‐mediated vasodilation in both groups, while prostacyclin contributed to maximal dilation in KD but not in WT. Femoral artery wall thickness of KD (20±1μm) at physiological pressure was smaller than that of WT (25±1μm; P<0.01, n=7), while constriction to phenylephrine was similar in both groups. Although KD and WT mice displayed similar metabolic parameters including fasting glucose level, KD mice showed a higher fasting insulin level (P<0.05, n=7–8). Conclusion Knock‐down of Angptl2 may lead to differences in the prostacyclin signaling pathway in the femoral arteries between the two genotypes of mice. Supported by CIHR MOP14496 and NSERC.