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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 7 of 7. This is the beginning of the thread.
Posted by theo on August 22, 2004, at 10:29:46
Article link for men trying Cymbalta.
http://www.menshealth.com/cda/article/0%2C2823%2Cs2-3-0-0-1332-3-1X2-3%2C00.html
Posted by Phil on August 23, 2004, at 10:19:57
In reply to Article for Men trying Cymbalta, posted by theo on August 22, 2004, at 10:29:46
Same BS Lexapro claimed.
Posted by linkadge on August 23, 2004, at 15:50:31
In reply to Re: Article for Men trying Cymbalta, posted by Phil on August 23, 2004, at 10:19:57
Any potent serotonin uptake inhibitor will cause anorgasmia, unless it has some 5-ht2 blockade which cymbalta does not have.
Linkadge
Posted by theo on August 23, 2004, at 18:56:12
In reply to Re: Article for Men trying Cymbalta, posted by linkadge on August 23, 2004, at 15:50:31
Then how can Prozac be prosexual for me, making me desire sex more than when I'm not on an SSRI/SNRI, and Paxil kills my sex drive? I guess my point is everything effects people in different ways, and I'm hoping Cymbalta effects me positively as Prozac did.
Posted by linkadge on August 23, 2004, at 19:31:52
In reply to Re: Article for Men trying Cymbalta » linkadge, posted by theo on August 23, 2004, at 18:56:12
Some people find that prozac is one of the better ones for sexual problems. Paxil seems to be the worst because of NO synthase inhibition. But prozac seems to be the best because it has a reasonable blockade of the 5-ht2c receptor can help some of the anorgazmia.
http://biopsychiatry.com/fluox5ht2c.htm
Linkadge
Posted by Dave001 on August 24, 2004, at 20:09:04
In reply to Re: Article for Men trying Cymbalta, posted by Phil on August 23, 2004, at 10:19:57
> Same BS Lexapro claimed.
Probably true.
J Pharmacol Exp Ther. 2004 Jul;310(1):141-9. Epub 2004 Mar 19.
Mechanisms for the inhibition of genital vascular responses by antidepressants in a female rabbit model.
Angulo J, Cuevas P, Cuevas B, Gupta S, De Tejada IS.
Antonio Robles, 4-9C, 28034 Madrid, Spain. isdtejada@terra.es
Vaginal and clitoral vasodilator responses (genital vascular responses; GVRs) to pelvic nerve electrical stimulation in female rabbits were measured by laser Doppler flow needle probes. The intravenous administration of various treatments was evaluated. GVRs were attenuated by a nitric-oxide synthase inhibitor (48.5 and 51.8% of control at 8 Hz in the vagina and clitoris, respectively) and norepinephrine (NE) (78.5 and 61.5%), whereas serotonin (5-HT) had no inhibitory effect. The selective 5-HT reuptake inhibitor (SSRI) escitalopram did not modify GVRs, whereas the SSRI paroxetine dose-dependently inhibited GVRs in female rabbits (43.3 and 53.1% at 5 mg/kg). GVRs were also significantly inhibited by the 5-HT and NE reuptake inhibitors venlafaxine (53.4 and 52.6% at 5 mg/kg) and duloxetine (40.9 and 37.4% at 1 mg/kg). l-arginine prevented the inhibitory effects of paroxetine (105.5 and 115.3%) and partially prevented duloxetine-induced reduction of GVRs but had no effect on the inhibition of GVRs induced by venlafaxine. Conversely, the alpha-adrenergic receptor blocker phentolamine had no effect on paroxetine-induced reduction of GVRs, partially prevented the inhibitory effects of duloxetine, and fully prevented the effects of venlafaxine (93.0 and 96.7%). Duloxetine-induced inhibition of GVRs was completely prevented by combined administration of l-arginine and phentolamine (123.5 and 103.6%). Although 5-HT or the highly selective SRI escitalopram did not inhibit GVRs, NE or inhibition of nitric oxide (NO) synthesis did. Inhibition of the NO pathway by paroxetine and duloxetine or activation of alpha-adrenergic mechanisms by venlafaxine and duloxetine lead to antidepressant-induced inhibition of GVRs in female rabbits.
PMID: 15034084
Posted by Dave001 on August 24, 2004, at 20:22:44
In reply to Re: Article for Men trying Cymbalta, posted by linkadge on August 23, 2004, at 19:31:52
> Some people find that prozac is one of the better ones for sexual problems. Paxil seems to be the worst because of NO synthase inhibition. But prozac seems to be the best because it has a reasonable blockade of the 5-ht2c receptor can help some of the anorgazmia.
>Paxil does seem to be the worst on paper, but according to the studies I have seen, escitalopram/citalopram seems to be the best of the SSRIs. (Es)citalopram is the only SSRI I have not seen evidence of causing NO inhibition. Granted, there are other mechanisms to take into account. See the abstract below and in my other post in this thread for reference to citalopram's apparent lack of peripheral NO inhibition.
Dave
Differential effects of serotonin reuptake inhibitors on erectile responses, NO-production, and neuronal NO synthase expression in rat corpus cavernosum tissue.
Br J Pharmacol 2001 Nov;134(6):1190-4 (ISSN: 0007-1188)
Angulo J; Peiro C; Sanchez-Ferrer CF; Gabancho S; Cuevas P; Gupta S; Saenz de Tejada I Fundacion para la Investigacion y el Desarrollo en Andrologia, Department de Investigacion, Hospital Ramon y Cajal, Madrid, Spain.
Increased incidence of impotence is associated with some selective serotonin-reuptake-inhibitors (SSRIs), but the pathophysiological mechanism is unknown. Paroxetine and citalopram are extensively used SSRIs, but only paroxetine has been shown to inhibit nitric oxide synthase (NOS) activity. NO is a key mediator of penile erection. Thus, the aim of this study was to determine the effects of paroxetine and citalopram on erectile function and NO production, in a rat model. Application of cavernosal nerve electrical stimulation produced frequency-related intracavernosal pressure (ICP) increases, which were inhibited by the NOS inhibitor, N(G)-nitro-L-arginine (0.3 mg x kg(-1)). Acute or chronic (2 weeks) paroxetine-treatment (10 mg x kg(-1)) reduced ICP-responses, while citalopram did not. Paroxetine, but not citalopram, significantly reduced nitrite+nitrate plasma levels by 61.4% and inhibited penile neuronal NOS (nNOS) protein expression by 31.2% after chronic treatment. The results show that paroxetine inhibits erectile responses in rats. We propose that this effect is due to reduced NO production and nNOS expression.
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