Abstract
Since there is evidence that paradoxical sleep deprivation (PSD) elicits penile erection (PE) and ejaculation (EJ), and that the erectile response of rats is mediated by nitric oxide, the present study sought to extend the latter finding by assessing the effects of sildenafil on the genital reflexes of male Wistar rats subjected to PSD. We also determined the influence of sildenafil on hormone concentrations. In the first experiment, sildenafil at doses ranging from 0.08 to 0.32 mg/kg was administered intraperitoneally to rats that had been deprived of sleep for 4 days and to home cage controls (N = 8-10/group). The frequency of PE and EJ was measured for 60 min. PSD alone induced PE in 50% of the animals; however, a single injection of sildenafil did not significantly increase the percentage of rats displaying PE compared to PSD-saline or to home cage groups. PSD alone also induced spontaneous EJ, but this response was not potentiated by sildenafil in the dose range tested. Testosterone concentrations were significantly lower in PSD rats (137 ± 22 ng/dL) than in controls (365 ± 38 ng/dL), whereas progesterone (0.9 ± 0.1 vs 5.4 ± 1 ng/mL) and plasma dopamine (103.4 ± 30 vs 262.6 ± 77 pg/mL) increased. These changes did not occur after sildenafil treatment. The data show that although sildenafil did not alter the frequency of genital reflexes, it antagonized hormonal (testosterone and progesterone) and plasma dopamine changes induced by PSD. The stimulation of the genital reflexes by sildenafil did not result in potentiating effects in PSD rats.
Highlights
It has been suggested that nitric oxide (NO) is the primary physiological mediator of penile erection (PE) [1,2]
We report the effects of paradoxical sleep deprivation (PSD) as an isolated factor on the occurrence of genital reflexes in male rats and corroborate previously findings showing that 50% of sleep-deprived rats displayed penile erection and 20% of them ejaculated [17]
Under the conditions of our experimental design, genital reflexes remained unchanged after sildenafil treatment in comparison to the PSD-saline group, indicating that the stimulation of the genital reflexes by sildenafil did not result in potentiating effects in PSD animals
Summary
It has been suggested that nitric oxide (NO) is the primary physiological mediator of penile erection (PE) [1,2]. It is generally accepted that NO originates in nonadrenergic noncholinergic nerve fibers of the penis, and is the principal vasodilator during the erectile response [6]. This response is abolished by systemic and intracerebroventricular administration of NO synthase inhibitors [6]. It enables an erection in response to sexual stimulation through selective inhibition of cyclic GMP-specific phosphodiesterase type 5 [7]. Erections occur through sexual stimulation of the parasympathetic nervous system leading to release of NO, a powerful vasodilator derived from the endothelial cells lining the corpus cavernosum. NO produces cyclic GMP, which causes the smooth muscle of the corpus cavernosum to relax and fill with arterial blood, producing the erection [8]
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