Molecular Mechanisms of Priapism Identified
Sickle cell disease-associated priapism tied to deficient erection control at a molecular level
FRIDAY, June 3 (HealthDay News) -- Recent advances have identified several molecular mechanisms, which may play a role in sickle cell disease-associated priapism, according to a review published online May 6 in The Journal of Sexual Medicine.
Trinity J. Bivalacqua, M.D., Ph.D., from the Johns Hopkins Medical Institutions in Baltimore, and colleagues reviewed literature from 2000 through 2010 to summarize recent advances in the understanding of molecular mechanisms of sickle cell disease-associated priapism. The most recent developments pertaining to the role of endothelial nitric oxide synthase, phosphodiesterase type 5 (PDE5), adenosine, RhoA/Rho-kinase (ROCK), and opiorphins in the pathophysiology of priapism were included.
The investigators found that recent advances have increased the understanding of the molecular pathogenesis of priapism. Novel developments indicate that priapism may result from altered vascular homeostatic actions in the penis, and may be correlated with deficient mechanisms of erection control on a molecular level. This includes abnormal signaling of the endothelium-derived nitric oxide and PDE5 signal transduction pathway in the penis. Dysfunctional regulatory control of signal transduction systems that interact with this pathway, such as adenosine and ROCK, may play a role in the development of priapism. Opiorphins are suggested to be involved in regulating corporal smooth muscle tone, thereby deregulating erection physiology.
"As the science underlying priapism further emerges, increasingly effective therapeutics for sickle cell disease-associated priapism is certain to follow," the authors write.