| First Author | Tanaka K | Year | 2011 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 31 |
| Issue | 5 | Pages | 1133-8 |
| PubMed ID | 21350197 | Mgi Jnum | J:191485 |
| Mgi Id | MGI:5461809 | Doi | 10.1161/ATVBAHA.110.218370 |
| Citation | Tanaka K, et al. (2011) Cytosolic phospholipase A2alpha contributes to blood pressure increases and endothelial dysfunction under chronic NO inhibition. Arterioscler Thromb Vasc Biol 31(5):1133-8 |
| abstractText | OBJECTIVE: Nitric oxide (NO) is an important modulator of cardiovascular function. In this study, we examined whether cytosolic phospholipase A2alpha (cPLA2alpha), an initial enzyme in the arachidonic acid pathway, is involved in blood pressure (BP) elevation in a murine model of chronic NO inhibition. METHODS AND RESULTS: cPLA2alpha gene-deficient mice (cPLA2alpha-/-) and wild-type mice (WT) were administered the NO synthesis inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) for 4 weeks. Before treatment, BP was comparable in both groups; it increased significantly in the WT but not in the cPLA2alpha-/- after treatment. Bone marrow transplantation experiments showed that cPLA2alpha in blood cells and plasma eicosanoid concentrations were not involved in BP elevation by L-NAME treatment. Activation of cPLA2alpha and subsequent production of eicosanoids in the aortic endothelium but not in aortic smooth muscle cell, heart, or kidney was observed after L-NAME treatment. Aortic ring assays revealed that endothelial function was comparable in both groups of mice before treatment. L-NAME treatment disturbed endothelial function in WT but not in cPLA2alpha-/-. CONCLUSIONS: These results suggest that endothelial cPLA2alpha may play a principal role in L-NAME-induced hypertension and may be a target molecule for maintaining endothelial function under NO inhibition. |
