Fig. 1
From: Pathophysiological effects of androgens on the female vascular system
Sex differences in the signal transduction pathways of eNOS activation in endothelial cells by testosterone and the subsequent vascular response. Testosterone is generally thought to increase nitric oxide (NO) availability through genomic and non-genomic pathways in men. Testosterone works through a separate pathway in women resulting in reduced NO availability and impaired vasodilation. Androgen receptor (AR), endothelial NO synthase (eNOS), extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase (PI3K), Akt (protein kinase B), G protein-coupled estrogen receptor 1 (GPR30 agonist, G-1). From Stanewicz et al. [7], with permission