Traditionally, testosterone and estrogen have been considered male and female sex hormones, respectively.
However, estradiol, the predominant form of estrogen, also plays a role in male sexual function.
Estradiol in men is essential for libido modulation, erectile function, and spermatogenesis.
Estrogen receptors, as well as aromatase, the enzyme that converts testosterone into estrogen, are abundant in the brain, penis and testicles, organs important for sexual function.
In the brain, estradiol synthesis increases in areas related to sexual arousal.
In addition, in the penis, estrogen receptors are found throughout the cavernous body with a high concentration around the neurovascular packages.
Low testosterone and high estrogen increase the incidence of erectile dysfunction independently of each other.
In the testicles, spermatogenesis is modulated at all levels by estrogen, beginning with the hypothalamus-pituitary-gonadal axis, followed by Leydig, Sertoli, and germ cells.
Ending with the ductal epithelium, epididymis and mature sperm.
The regulation of testicular cells by estradiol shows both inhibitory and stimulating influence, indicating an intricate tuning of dose-dependent and temporarily sensitive modulation.
Therefore, estradiol plays an overall contribution to male sexual function by observing the effects of the hormone on erectile function, spermatogenesis and libido.
Either way, depending on their values in the blood and in the target organs.
On the other hand, estrogens produce an increase in sex hormone-transporting globulin (SHBG) which is a synthesized glycoprotein in the liver whose biological function is the transport of steroid sex hormones.
Mainly testosterone and to a lesser degree of affinity to estradiol, thus preventing the degradation of steroid sex hormones.
But on the other hand, they reduce free testosterone, which is really effective or bioavailable.
Both endogenous and environmental estrogens may be responsible for this increase in SHBG.
SHBG levels correlate with measures of severity of heart failure and are associated with an increased risk of cardiac death.
However, the links between endocrine and cardiovascular function have not been taken into account for many years.
There is growing evidence that the myocardium, similarly to all tissues and organs of the body, is under constant hormonal influences.
For male fertility to occur, there must be a balance between testosterone and estradiol (and not any estrogen) and the relationship: total testosterone/estradiol may be useful in the study of the infertile male.
Keywrords: testosterone-estradiol and fertility ratio, SHBG and myocardium, endocrine and cardiovascular function, increased estrogens and SHBG, free testosterone and estrogens, estradiol and male sexual function, estradiol and spermatogenesis, estradiol and Leydig cell, estradiol and Sertoli cell, estradiol and germ cell, estradiol and arousal, estradiol and aromatase.