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Objective— Nitric oxide (NO) is an important modulator of cardiovascular function. In this study, we examined whether cytosolic phospholipase A2 α (cPLA2 α), 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— cPLA2 α gene–deficient mice (cPLA2 α−/−) and wild-type mice (WT) were administered the NO synthesis inhibitorN ω -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 cPLA2 α−/− after treatment. Bone marrow transplantation experiments showed that cPLA2 α in blood cells and plasma eicosanoid concentrations were not involved in BP elevation byl -NAME treatment. Activation of cPLA2 α and subsequent production of eicosanoids in the aortic endothelium but not in aortic smooth muscle cell, heart, or kidney was observed afterl -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 cPLA2 α−/−.Conclusion— These results suggest that endothelial cPLA2 α may play a principal role inl -NAME-induced hypertension and may be a target molecule for maintaining endothelial function under NO inhibition.

Cytosolic Phospholipase A 2 α Contributes to Blood Pressure Increases and Endothelial Dysfunction Under Chronic NO Inhibition

Cytosolic Phospholipase A ₂ α Contributes to Blood Pressure Increases and Endothelial Dysfunction Under Chronic NO Inhibition