H ₂ S Protects Against Pressure Overload–Induced Heart Failure via Upregulation of Endothelial Nitric Oxide Synthase

Abstract

Our results demonstrate that H2S levels are decreased in mice in the setting of heart failure. Moreover, CSE plays a critical role in the preservation of cardiac function in heart failure, and oral H2S therapy prevents the transition from compensated to decompensated heart failure in part via upregulation of endothelial nitric oxide synthase and increased nitric oxide bioavailability.