Abstract
Background and Aims: Pulmonary endothelial cell (EC) dysfunction leads nitric oxide synthase (NOS) uncoupling and release of vasoconstrictors like angiotensin II and endothelin-1. The omega-3 fatty acid (n3FA) eicosapentaenoic acid (EPA) reduced cardiovascular (CV) events in high-risk patients (REDUCE-IT) but the mechanism is not understood. We tested EPA on expression of proteins that modulate NOS, including caveolin-1 and heat shock protein-90 (Hsp90), and proteins that effect vasoconstriction, including endothelin-converting enzme-1 (ECE-1) and angiotensin converting enzyme (ACE).
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