Nitric oxide inhibits RhoA/Rho-kinase signaling to cause penile erection

Thomas M. Mills, Kanchan Chitaley, Ronald W. Lewis, R. Clinton Webb

Research output: Contribution to journalArticle

67 Scopus citations

Abstract

The RhoA/Rho-kinase pathway mediates vasoconstriction in the cavernosal circulation. Inhibition of this pathway leads to penile erection in the in vivo rat model. These studies examined the hypothesis that nitric oxide (NO) inhibits RhoA/Rho-kinase signaling as part of normal erection. The results show that NO causes increased intracavernosal pressure and that this response is potentiated by prior treatment with a threshold dose of the Rho-kinase inhibitor, (+)-(R)-trans-4-(1-Aminoethyl)-N-(4-pyridyl) cyclohexanecarboxamide dihydrochloride, monohydrate (Y-27632). These results support the hypothesis that NO inhibits Rho-kinase-induced cavernosal vasoconstriction during erection.

Original languageEnglish (US)
Pages (from-to)173-174
Number of pages2
JournalEuropean Journal of Pharmacology
Volume439
Issue number1-3
DOIs
StatePublished - Mar 29 2002

Keywords

  • Nitric oxide (NO)
  • Penile erection
  • RhoA/Rho-kinase

ASJC Scopus subject areas

  • Pharmacology

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