Interesting Info On Erection

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Excerpts from: Erectile dysfunction: management update
Luke Fazio and Gerald Brock
From the Division of Urology, Faculty of Medicine and Dentistry, University of Western Ontario, London, Ont.


Interesting info

Three mechanisms trigger these vascular changes: psychogenic, reflexogenic and centrally originated (nocturnal erections). Psychogenic erections occur through stimulatory pathways (e.g., sound, smell, sight and touch) that travel from the spinal erection centres (T11–L2 and S2–S4) and induce a dopaminergic initiation of erection from the medial pre-optic area. Reflexogenic erections, induced by direct genital stimulation, send ascending messages to the central erection centres and direct messages to the autonomic nuclei, which explains residual erectile activity in patients with upper spinal cord injuries. Nocturnal erections, initiated in the pontine reticular formation and amygdalae, are seen during REM sleep and are believed to be caused by a relative decrease in sympathetic inhibition with augmentation of the pro-erectile centres.

Despite considerable recent experimentation in animal models and human volunteers, information on the central pathways of erection remains cursory at best. It is known that androgens play a predominantly modulating role by their effect on libido and sexual behaviour. Testosterone enhances sexual interest and the frequency of sexual acts; it increases the frequency of nocturnal erections but does not effect reflexogenic or psychogenic erections.

More on how Viagra & Cialis Work

The use of oral therapy has long been preferred over invasive procedures such as injection therapy for erectile dysfunction. We review the pharmacology, efficacy and side effects of the newest agents available for oral therapy: the PDE-5 inhibitors sildenafil, vardenafil and tadalafil.

PDE-5 is an enzyme found in trabecular smooth muscle. It catalyzes the degradation of cGMP, which results in an elevated cytosolic calcium concentration and smooth-muscle contraction . PDE-5 inhibitors, therefore, block this biochemical pathway to promote erection. Eleven subtypes of PDEs have been described, with 30 isoenzymes mediating a variety of physiologic actions throughout the body.32 PDEs exhibit enormous functional diversity; at present, our understanding of PDE types 1 to 6 are considerably better than our understanding of PDE types 7 to 11.

All 3 of the PDE-5 inhibitors are metabolized by the cytochrome P-450 3A4 enzyme. Sildenafil and vardenafil share similar pharmacokinetic properties. Both have been shown in clinical trials to improve the ability to attain and maintain erections when taken 1 hour before sexual activity. Since sildenafil was introduced, extensive clinical experience has been gained with prescriptions of it to more than 20 million patients. Vardenafil has distinguished itself by demonstrating efficacy in patients who have previously undergone radical prostatectomy for localized prostate cancer (a group that had been difficult to treat because of nerve and vascular injury secondary to surgery) and in patients with diabetes.

Tadalafil differs from sildenafil and vardenafil in its chemical structure and its lack of inhibition of PDE type 6. Tadalafil exhibits a prolonged half-life of 17.5 hours, and the time to peak concentration is about 2.0 (range 0.5–12.0) hours in healthy volunteers.37 Among men with erectile dysfunction, a significantly higher percentage of attempts at sexual intercourse were successful up to 24–36 hours after use of tadalafil compared with placebo. The pharmacokinetics of tadalafil is not clinically influenced by food or alcohol intake, or by intrinsic factors such as diabetes, or renal or hepatic impairment.

http://www.cmaj.ca/cgi/content/full/170/9/1429/T232

http://www.cmaj.ca/cgi/content/full/170/9/1429/T332