Therapeutically Relevant Concentrations of Raloxifene Dilate Pressurized Rat Resistance Arteries via Calcium-Dependent Endothelial Nitric Oxide Synthase Activation

Abstract

Raloxifene at therapeutically relevant concentrations inhibits myogenic constriction by an NO-dependent mechanism that causally involves the elevated [Ca(2+)](i) in endothelial cells and subsequent eNOS activation. Raloxifene dilates resistance arteries more effectively in female rats, indicating its significant gender-related action on endothelial cells in microcirculation.