In contrast, 5β-DHT is devoid of genomic androgenic activity at the androgen receptor, but is a highly potent and efficacious nongenomic vasodilator in vitro and in vivo [31, 36] and tissue levels of the enzyme that converts TES to 5β-DHT (5β-reductase) are reduced in patients with essential hypertension [51]. This evidence concerns the gene AR and essential hypertension.