Vasoconstriction, RhoA/Rho-kinase and the erectile response

T. M. Mills, R. W. Lewis, C. J. Wingard, A. E. Linder, L. Jin, R. C. Webb

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


Recent studies have suggested that contraction of the smooth muscle in the cavernosal arterioles and in the walls of the cavernosal sinuses is maintained by the RhoA/Rho-kinase signaling pathway. However, this contraction activity must be overcome to permit the vasorelaxation essential for erection. We postulate that nitric oxide (NO) causes erection primarily by inhibiting the RhoA/Rho-kinase pathway. The following will discuss evidence in support of the important role of Rho-kinase-mediated vasoconstriction in the nonerect penis and how NO overrides this Rho-kinase-mediated vasoconstriction to permit vasodilation and erection.

Original languageEnglish (US)
Pages (from-to)S20-S24
JournalInternational journal of impotence research
StatePublished - Oct 2003
Externally publishedYes


  • Nitric oxide
  • Penile erection
  • Rho-kinase

ASJC Scopus subject areas

  • Urology


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