Priapism (prolonged penile erection in the absence of sexual interest) is common in male individuals with sickle cell disease (SCD), a blood disorder characterized by abnormally shaped red blood cells.
Priapism is considered a medical emergency because it is associated with decreased blood flow to the erectile tissue, which can result in erectile tissue damage and, subsequently, erectile dysfunction and impotence.
However, the development of effective treatment and prevention approaches has been limited by poor understanding of the molecular mechanisms underlying the condition. Some insight into this has now been provided by Yang Xia and colleagues, at the University of Texas Medical School at Houston, who have shown that male mice lacking the protein ADA, which breaks down the molecule adenosine, exhibit priapism that could be corrected by ADA therapy.
Further analysis indicated that high levels of adenosine induced priapism through stimulation of the A2B adenosine receptor in ADA-deficient mice. As increased adenosine signaling through the A2B adenosine receptor was also shown to contribute to priapism in SCD transgenic mice, which are a well-accepted mouse model of the condition, the authors suggested that approaches to either reduce adenosine levels or block A2B adenosine receptor activation might provide new ways to treat priapism.
Journal reference: Excess adenosine in murine penile erectile tissues contributes to priapism via A2B adenosine receptor signaling. Journal of Clinical Investigation. March 13, 2008.
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