Sexual medicine
Atorvastatin improves hyperlipidemia-induced erectile dysfunction via PKA-associated eNOS phosphorylation at the Ser633 site
By Zhang X, Wang X, Zhang Z and 4 others.
Abstract
Introduction
Hyperlipidemia contributes to vasculogenic erectile dysfunction (ED) by reducing endothelial nitric oxide bioavailability. Although atorvastatin has been reported to improve ED, the upstream mechanism by which it restores endothelial nitric oxide synthase (eNOS) activity remains unclear. This study aimed to evaluate the therapeutic effect of atorvastatin in hyperlipidemia-induced erectile dysfunction (HLED) and to determine whether protein kinase A (PKA)-associated phosphorylation of eNOS at Ser633 contributes to this effect.
Methods
Hyperlipidemia-induced erectile dysfunction was induced in rats by a high-fat diet. Animals received low- or high-dose atorvastatin, with tadalafil as a positive control. Erectile function, serum lipid profiles, oxidative stress, penile fibrosis, and cavernosal eNOS signaling were assessed. In parallel, oxidized low-density lipoprotein (ox-LDL)-injured rat corpus cavernosum endothelial cells (RCECs) were treated with atorvastatin in the presence or absence of the PKA inhibitor H89.