{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T03:43:20Z","timestamp":1787024600137,"version":"build-2736575974"},"reference-count":59,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2013,1,2]],"date-time":"2013-01-02T00:00:00Z","timestamp":1357084800000},"content-version":"vor","delay-in-days":1827,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Andrology"],"published-print":{"date-parts":[[2008,1,2]]},"abstract":"<jats:p>\n                    <jats:bold>ABSTRACT:<\/jats:bold>\n                    Spontaneously hypertensive rats (SHR) are characterized by impaired erectile function and overactivity of the procontractile RhoA\/Rho\u2010associated, coiled\u2010 coil\u2014containing protein kinase (RhoA\/ROCK) pathway, as compared with their normotensive counterpart, Wistar\u2010Kyoto rats. By measuring the intracavernous pressure:mean arterial pressure (ICP:MAP) ratio after electrostimulation of the cavernous nerve, we confirmed these findings and showed that responsiveness to sildenafil (25 mg\/kg by oral gavage) also is hampered in SHR. A 2\u2010week treatment with atorvastatin (5 and 30 mg\/kg) improved the sildenafil\u2010induced ICP:MAP increase and normalized RhoA and ROCK2 overexpression in SHR corpora cavernosa (CC). Conversely, other genes, neuronal nitric oxide synthase (NOS), endothelial NOS, and phosphodiesterase 5, were unaffected. In human fetal smooth muscle cells derived from CC (hfPSMC), atorvastatin inhibited RhoA membrane translocation and ROCK activity, as well as RhoA\u2010dependent biologic functions like cell migration and cell proliferation. Atorvastatin's effect on migration was rescued in a dose\u2010dependent manner by geranylgeranyl pyrophosphate, suggesting the involvement of RhoA geranylgeranylation. In hfPSMC, atorvastatin decreased the expression of RhoA\u2010dependent genes such as\n                    <jats:italic>ROCK2<\/jats:italic>\n                    , desmin, \u03b1\u2010smooth muscle actin, SM22\u03b1, and myocardin. In contrast to atorvastatin, elocalcitol, a vitamin D analog that also interferes with RhoA activation in SHR bladder, was unable to restore penile responsiveness to sildenafil. In conclusion, atorvastatin, but not elocalcitol, ameliorates sildenafil\u2010induced penile erections in SHR, likely by interfering with RhoA\/ROCK signaling within the penis.\n                  <\/jats:p>","DOI":"10.2164\/jandrol.107.003152","type":"journal-article","created":{"date-parts":[[2007,12,21]],"date-time":"2007-12-21T18:52:44Z","timestamp":1198263164000},"page":"70-84","source":"Crossref","is-referenced-by-count":44,"title":["Atorvastatin But Not Elocalcitol Increases Sildenafil Responsiveness in Spontaneously Hypertensive Rats by Regulating the RhoA\/ROCK 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