Hypertension is a chronic disorder that contributes to cardiovascular disease (World Health, 2009). Currently, it is the major cause of morbidity and mortality in people worldwide (James et al., 2014). Hypertension associated with sexual dysfunction has been reported in male patients with hypertension (Fogari et al., 2001). Additionally, decreased sexual activity has been observed in male patients with essential hypertension, which has been associated with reduced testosterone levels (Fogari et al., 2002). A previous study has reported that serum total testosterone and epididymal sperm motility are significantly reduced in rats with nitric oxide (NO) depletion (Adedara et al., 2018). It is well known that testosterone is an essential hormone for the initiation and maintenance of spermatogenic processes (Chauhan et al., 2007), synthesised by testicular Leydig cells using cholesterol as its substrate (Li et al., 2011). The biosynthesis of testosterone requires steroidogenic acute regulatory protein (StAR), a mitochondrial cholesterol transporter, that transfers lipids from outside the mitochondrial membrane to the inside (Stocco, 2001). Reportedly,