Elevated RhoA/Rho-kinase activity in the aged rat penis: mechanism for age-associated erectile dysfunction Liming Jin 1 , Tongyun Liu 1 , Gwen A. Lagoda, Hunter C. Champion, Trinity J. Bivalacqua and Arthur L. Burnett 2 Department of Urology, Johns Hopkins University, Baltimore, Maryland, USA 2 Correspondence: Department of Urology Johns Hopkins University Baltimore, MD 21287, USA. E-mail: aburnett@jhmi.edu <h3>SPECIFIC AIMS</h3> Epidemiologic studies have shown that aging accounts significantly for the prevalence of erectile dysfunction (ED). The pathophysiology of ED during aging and its underlying molecular mechanisms are largely unknown. Evidence has shown that the RhoA/Rho-kinase signaling pathway maintains constriction of the cavernosal arterioles and sinuses, keeping the penis in the flaccid state. The aim of this study is to test the hypothesis that increased RhoA/Rho-kinase signaling pathway is a major factor in the pathogenesis of age-associated ED and the mechanism involves increased penile smooth muscle contractility through inhibition of myosin light chain phosphatase targeting subunit (MYPT1). <h3>PRINCIPAL FINDINGS</h3> <h3>1. Erectile function was impaired in aged rats</h3> Erectile function was determined by measuring intracavernosal pressure (ICP), mean arterial pressure (MAP) and total ICP in young and aged rats upon electrical stimulation of the cavernous nerve. Erectile responses were significantly
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Elevated RhoA/Rho-kinase activity in the aged rat penis: mechanism for age-associated erectile dysfunction
Jin, Liming; Liu, Tongyun; Lagoda, Gwen A.; Champion, Hunter C.; Bivalacqua, Trinity J.; Burnett, Arthur L.
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, Volume 20 (3): 536
Fed of American Socs for Experimental Biology – Mar 1, 2006
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