Chronic Lexapro ED mechanism

[brman]

Chronic Lexapro ED mechanism - OP <Fun

Chronic Escitalopram Treatment Induces Erectile Dysfunction by Decreasing Nitric Oxide Bioavailability Mediated by Increased Nicotinamide Adenine Dinucleotide Phosphate Oxidase Activity and Reactive Oxygen Species Production
Modar Kassan, George F. Lasker, Suresh C. Sikka, Sree Harsha Mandava, Ahmet Gokce, Khalid Matrougui, Wayne J.G. Hellstrom, Philip J. Kadowitzemail address, Ege Can Serefoglu
Received 20 May 2013; accepted 26 July 2013.

Abstract Full Text PDF Images References
Objective
To investigate the effects of escitalopram, a selective serotonin reuptake inhibitor, on erectile and penile vascular function in the rat.

Methods
The effect of chronic treatment with escitalopram (0.286 mg/kg/day) on change in intracavernosal pressure, maximum intracavernosal pressure/mean arterial pressure, and area under the intracavernosal pressure curve in response to cavernosal nerve stimulation was measured. The effect of chronic escitalopram treatment on endothelial-dependent relaxant responses was investigated in isolated mesenteric and internal pudendal resistance arteries. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and nitric oxide synthase levels were determined with enzymatic assay and Western blot, respectively.

Results
Chronic treatment with escitalopram resulted in a significant reduction in the erectile response to cavernosal nerve stimulation without an effect on the response to intracavernosal injection of the nitric oxide donor sodium nitroprusside. The decrease in erectile function was associated with marked increases in NADPH oxidase activity in the corpora cavernosa. Treatment with escitalopram also caused a significant reduction in the relaxant response to acetylcholine in isolated internal pudendal and mesenteric resistance arteries without altering the response to sodium nitroprusside. The decreased response to acetylcholine in the isolated vascular segments was associated with a marked increase in NADPH oxidase activity that was corrected by treatment with the NAPDH oxidase inhibitor apocynin.

[brman]

OP <Fun

I doubt this effect is specific to escitalopram and is likely a result serotonin excess in the periphery. NADPH activity appears to be upregulated by SSRIs thus limiting NO availability. And that is without tampering with the expression of NO synthase. I'm currently looking for OTC NADPH inhibitors and I urge you all to join me. Epicatechin might be.