Sildenafil for Women Patients With Antidepressant-Induced Sexual Dysfunction

Nurnberg, H. George; Hensley, Paula L.; Parker, Lynda M.; Keith, Samuel J.

doi:10.1176/ps.50.8.1076

Cited by 76 publications

(38 citation statements)

References 6 publications

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“…10 On the other hand, treatment with PDE5 inhibitors could alleviate the sexual dysfunction secondary to SSRI administration, as reported in case reports in male patients 17 and preliminary clinical trials in females treated with sildenafil. 18 This concept is supported by the results of the present study, which demonstrates that treatment with the new PDE5 inhibitor, vardenafil is able to reverse completely the erectile dysfunction experimentally induced by paroxetine administration, providing a rationale for the use of PDE5 inhibitors in the treatment of erectile dysfunction secondary to treatment with SSRIs.…”

Section: Discussionsupporting

confidence: 73%

Vardenafil reverses erectile dysfunction induced by paroxetine in rats

Angulo¹,

Bischoff

Gabancho³

et al. 2003

Int J Impot Res

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Selective serotonin reuptake inhibitors (SSRIs) are associated with a high incidence of impotence. Paroxetine is an extensively used SSRI that has been shown to impair erectile function in patients, to induce erectile dysfunction and to inhibit nitric oxide synthase (NOS) activity and NO production in animal models. NO is a key mediator of penile erection. Vardenafil is a type 5 phosphodiesterase inhibitor that potentiates NO-mediated responses in isolated trabecular smooth muscle and penile erection in men in clinical trials. The aim of this study was to evaluate the effects of vardenafil on the impairment of erectile responses produced by paroxetine in the rat model. Application of cavernosal nerve electrical stimulation (CNES) produced frequency-related intracavernosal pressure (ICP) increases, which were inhibited by the NOS inhibitor N G -nitro-l-arginine (0.3 mg/kg) and potentiated by vardenafil (0.3 mg/kg). Acute paroxetine treatment (10 mg/kg) significantly reduced ICP-responses to CNES. This inhibition was completely reversed by vardenafil (0.3 mg/kg) administration. The results show that the erectile dysfunction induced by paroxetine in rats can be effectively treated with vardenafil, suggesting that the use of this compound could be a reasonable therapeutic approach to treating erectile dysfunction associated with SSRI administration.

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Section: Discussionsupporting

confidence: 73%

Vardenafil reverses erectile dysfunction induced by paroxetine in rats

Angulo¹,

Bischoff

Gabancho³

et al. 2003

Int J Impot Res

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show abstract

“…9,[21][22][23] Although the preliminary results were not satisfactory in postmenopausal women treated with the PDE5 inhibitor sildenafil, 24 maybe because of the poor expression of NOS in the vaginal wall of these women, 17 additional encouraging results have been obtained with this drug in selected cohorts. [25][26][27] In conclusion, further research efforts are needed to augment the knowledge of the physiology and pathophysiology of female sexual function, including the development of animal models for the evaluation of new therapeutic approaches to treat sexual dysfunction. The results obtained in this study demonstrate that vardenafil enhances the sexual vascular response in anesthetized female dogs.…”

Section: Discussionmentioning

confidence: 99%

Vardenafil enhances clitoral and vaginal blood flow responses to pelvic nerve stimulation in female dogs

Angulo

Cuevas

et al. 2003

Int J Impot Res

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The relaxation of the smooth muscle in the vagina and clitoris and the increase of blood flow into these organs is thought to be essential in the female sexual response. Vardenafil is a type 5 phosphodiesterase (PDE5) inhibitor that potentiates the nitric oxide (NO)/cGMP pathway facilitating penile smooth muscle relaxation and improving penile erection in men. Although the potentiation of the NO/cGMP pathway through PDE5 inhibitors can clearly enhance blood flow into the penis and is used in the therapy of male sexual dysfunction, there is controversy about the efficacy of these agents in improving female sexual function. The aim of this work was to evaluate the effects of vardenafil on the increase of blood flow into the vagina and clitoris induced by pelvic nerve electrical stimulation (PNES) in a female dog model. Application of PNES produced consistent and frequency-related increased blood flow into the vagina and clitoris of anesthetized female dogs. The magnitude and duration of the blood flow responses to PNES were variable among the different animals but remained stable over time within the same animal. The intravenous administration of vardenafil (1 mg/kg) significantly potentiated the increases in blood flow produced by PNES into the vagina (381.4 and 206.2% of control response at 5 and 10 Hz, respectively, Po0.01, n ¼ 6) and clitoris (379.4 and 238.5% of control response at 5 and 10 Hz, respectively, Po0.01, n ¼ 6) 20 min after administration. The significant enhancement of PNESinduced responses was maintained 50 min (224.5 and 181.0%, Po0.01 in vagina; 294.8 and 258.9%, Po0.05 in clitoris) and 80 min after vardenafil administration (209.5 and 156.9%, Po0.05 in vagina; 268.9 and 194.9%, Po0.05 in clitoris). Here we present a feasible model for research into female sexual function. Our results show that vardenafil effectively potentiates the blood flow responses to PNES in the genitalia of female dogs. These results emphasize the role of the NO/cGMP pathway in the local vasodilatory response in female sexual organs and provide a rationale for testing PDE5 inhibitors, such as vardenafil, as a treatment for certain forms of female sexual dysfunction.

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“…Several drugs with different mechanisms have been used to restore such symptoms. Those agents have effects on dopaminergic (Masand et al, 2001), serotonergic (Landen et al, 1999), noradrenergic (Hollander and McCarley, 1992) or both noradrenergic and specific serotonergic (Koutouvidis et al, 1999) receptors, or local effects on blood flow in the genitals (Nurnberg et al, 1999). Mirtazapine blocks postsynaptic 5-HT2 and 5-HT3 receptors and has an antagonistic effect on presynaptic a-2 adrenergic autoreceptors and heteroreceptors (Saiz-Ruiz et al, 2005;Stimmel et al, 1997).…”

Section: Introductionmentioning

confidence: 99%