Title

Role of adenosine signaling in penile erection and erectile disorders.

Publication Date

11-1-2010

Journal

J Sex Med. 2010 November; 7(11): 3553–3564.

Abstract

INTRODUCTION: Penile erection is a hemodynamic process, which results from increased flow and retention of blood in the penile organ due to the relaxation of smooth muscle cells. Adenosine, a physiological vasorelaxant, has been shown to be a modulator of penile erection.

AIM: To summarize the research on the role of adenosine signaling in normal penile erection and erectile disorders.

MAIN OUTCOME MEASURES: Evidence in the literature on the association between adenosine signaling and normal and abnormal penile erection, i.e., erectile dysfunction (ED) and priapism.

METHODS: The article reviews the literature on the role of endogenous and exogenous adenosine in normal penile erection, as well as in erectile disorders namely, ED and priapism.

RESULTS: Adenosine has been shown to relax corpus cavernosum from various species including human in both in vivo and in vitro studies. Neuromodulatory role of adenosine in corpus cavernosum has also been demonstrated. Impaired adenosine signaling through A(2B) receptor causes partial resistance of corpus cavernosum, from men with organic ED, to adenosine-mediated relaxation. Increased level of adenosine has been shown to be a causative factor for priapism.

CONCLUSION: Overall, the research reviewed here suggests a general role of exogenous and endogenous adenosine signaling in normal penile erection. From this perspective, it is not surprising that impaired adenosine signaling is associated with ED, and excessive adenosine signaling is associated with priapism. Adenosine signaling represents a potentially important diagnostic and therapeutic target for the treatment of ED and priapism.

Keywords

Adenosine, Humans, Impotence, Vasculogenic, Male, Penile Erection, Penis, Priapism, Receptors, Cyclic AMP, Receptors, Neurotransmitter, Receptors, Purinergic P1, Risk Factors, Signal Transduction, Vasodilator Agents



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