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

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29 Scopus citations

Abstract

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
Volume15
DOIs
StatePublished - Oct 2003

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Keywords

  • Nitric oxide
  • Penile erection
  • Rho-kinase

ASJC Scopus subject areas

  • Urology

Cite this

Mills, T. M., Lewis, R. W., Wingard, C. J., Linder, A. E., Jin, L., & Webb, R. C. (2003). Vasoconstriction, RhoA/Rho-kinase and the erectile response. International journal of impotence research, 15, S20-S24. https://doi.org/10.1038/sj.ijir.3901068