Do therapeutically relevant concentrations of raloxifene dilate pressurized rat resistance arteries via calcium-dependent endothelial nitric oxide synthase activation?
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.
Radiographic properties of sinus opacities suggest the nature of sinus opacities are related not only to some common underlying pathology but also to factors related to the specific sinus as well as other spatially close affected sinuses. This suggests an anatomic orientation for sinus pathophysiology in CRS.