Penile erection and cardiac risk: pathophysiologic and pharmacologic mechanisms

Abstract

Erection is initiated through the parasympathetic nervous system, activation of which overrides the sympathetic tone that maintains the penis in a nonerectile (flaccid) state. This state is maintained mainly through the release of norepinephrine from penile adrenergic nerves. Norepinephrine contracts the vasculature and cavernosal smooth muscle. Arousal/erection is associated with a decrease of norepinephrine release in the penis, with a release of nitric oxide, and with a reduction in penile smooth muscle tone. It is also associated with minor cardiovascular changes. Heart rate increases by 4–8 beats per minute, on average, and the rate–pressure product and oxygen consumption increase by approximately 25%. There may be no changes in systemic venous norepinephrine concentrations; systemic venous epinephrine concentrations increase by about 60%. Drugs initiating or enhancing erection act by inhibiting norepinephrine-induced contraction (e.g., phentolamine) or by enhancing or directly inducing relaxation of the corpora cavernosa and the penile vasculature (e.g., sildenafil). Despite potentially negative hemodynamic actions when given parenterally, oral phentolamine—in doses required for enhancing erection—appears to produce few cardiovascular adverse effects. The hemodynamic effects of sildenafil are small, even in patients with coronary artery disease. However, the effects of the drug on human myocardium have not been conclusively established, and should be further investigated. As judged by available information, the cardiac risk associated with erection, with or without enhancement of drugs currently used for treatment of erectile dysfunction, is low.