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Vasoconstriction, RhoA/Rho-kinase and the erectile response

International Journal of Impotence Research volume 15, pages S20–S24 (2003)Cite this article

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.

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Authors and Affiliations

  1. Department of Physiology, Medical College of Georgia, Augusta, Georgia, USA

    T M Mills, C J Wingard, A E Linder, L Jin & R C Webb

  2. Department of Surgery (Urology), Medical College of Georgia, Augusta, Georgia, USA

    T M Mills, R W Lewis, C J Wingard & R C Webb

Authors
  1. T M Mills
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  2. R W Lewis
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  3. C J Wingard
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  4. A E Linder
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  5. L Jin
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  6. R C Webb
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Correspondence to T M Mills.

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Mills, T., Lewis, R., Wingard, C. et al. Vasoconstriction, RhoA/Rho-kinase and the erectile response. Int J Impot Res 15 (Suppl 5), S20–S24 (2003). https://doi.org/10.1038/sj.ijir.3901068

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  • DOI: https://doi.org/10.1038/sj.ijir.3901068

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