Estradiol is an independent risk factor for organic erectile dysfunction in eugonadal young men.

Erectile dysfunction attributable to testosterone deficiency is less common in young males, and the effect of estradiol on erectile function in eugonadal young males is unclear. We analyzed data from 195 male participants, including 143 eugonadal patients with erectile dysfunction and 52 healthy men. To distinguish psychogenic and organic erectile dysfunction, penile rigidity was measured using the nocturnal penile tumescence rigidity test. Serum levels of sexual hormones were quantified by electrochemiluminescence, and penile vascular status was assessed by penile color Doppler ultrasound. Both serum estradiol levels and the ratio of estradiol to testosterone were higher in patients with organic erectile dysfunction than in patients with psychogenic erectile dysfunction or healthy controls. Organic erectile dysfunction was negatively associated with estradiol levels and the ratio of estradiol to testosterone, and estradiol was the only significant risk factor for organic erectile dysfunction (odds ratio: 1.094; 95% confidence interval: 1.042-1.149, P = 0.000). Moreover, serum estradiol levels were negatively correlated with penile rigidity. Serum estradiol levels were higher and penile rigidity was lower in patients with venous erectile dysfunction than in patients with nonvascular erectile dysfunction. We conclude that elevated serum estradiol levels may impair erectile function and may be involved in the pathogenesis of organic erectile dysfunction in eugonadal young men.

[Effect of nitric oxide donor and alpha1-receptor antagonist on proliferation/apoptosis of hyperplastic prostatic stromal cells in vitro].

OBJECTIVE: To study the effect of nitric oxide donor and alpha(1)-receptor antagonist on proliferation/apoptosis of hyperplastic prostatic stromal cells in vitro. METHODS: Primary cultured prostatic stromal cells were treated by nitric oxide donor SNP and Terazosin, and the antiproliferative index and apoptosis index were determined by MTT assay and TUNEL respectively. RESULTS: There was a significant dose-effect relationship between SNP and the antiproliferative effects, while Terazosin showed no antiproliferative effects and the combination of SNP and Terazosin showed no strengthen effects. Terazosin significantly induced apoptosis, but SNP showed no effect on induction of apoptosis, while there were much more effects of inducing apoptosis in the combination of Terazosin and SNP than the Terazosin alone. CONCLUSIONS: Terazosin induces apoptosis in cultured BPH stromal SMCs with little effect on the cell proliferation. SNP inhibits the proliferation of the cells without affecting apoptosis. The apoptosis induction effect is enhanced when Terazosin is combined with SNP, but they do not have an additive antiproliferative effect.