Endothelial Relaxation Mechanisms and Oxidative Stress Are Restored by Atorvastatin Therapy in Ovariectomized Rats

摘要: The studies on hormone replacement therapy (HRT) in females with estrogen deficiency are not conclusive. Thus, non-estrogen therapies, such as atorvastatin (ATO), could be new strategies to substitute or complement HRT. This study evaluated the effects of ATO mesenteric vascular bed (MVB) function from ovariectomized (OVX) female rats. Female rats were divided into control SHAM, OVX, and OVX treated 17β-estradiol (EST) groups. MVB reactivity was determined organ chambers, oxidative stress by dihydroethidine staining, expression target proteins western blot. reduction acetylcholine-induced relaxation restored EST treatment. endothelium-dependent nitric oxide (NO) component reduced rats, whereas endothelium-derived hyperpolarizing factor (EDHF) prostanoids altered MVBs. Endothelial dysfunction associated stress, an up-regulation iNOS NADPH oxidase a down-regulation eNOS expression. Treatment improved NO normalized those signaling pathways enzymes. protective effect endothelial caused highlights significant therapeutic benefit for statins independent its cholesterol, thus providing evidence that used cardiovascular estrogen-deficient state, menopause.