The ups and downs of Rho-kinase and penile erection: upstream regulators and downstream substrates of rho-kinase and their potential role in the erectile response

Int J Impot Res. 2003 Apr;15(2):105-9. doi: 10.1038/sj.ijir.3900964.

Abstract

In the absence of arousal stimuli, the activity of the Rho-kinase-mediated signaling pathway promotes vasoconstriction of the cavernosal arterioles and sinuses, keeping the penis in the nonerect state. Upon sexual arousal or during nocturnal tumescence, nitric oxide (NO), released from nonadrenergic/noncholinergic nerves or from local endothelial cells, induces cavernosal vasodilation, resulting in an elevation in blood flow and intracavernosal pressure to initiate the erectile response. Although NO is thought to be the principal stimulator of penile erection, the signaling mechanism(s) of NO-mediated cavernosal vasodilation is unknown. In this article, we will consider the novel hypothesis that NO induces penile erection through the inhibition of endogenous Rho-kinase-mediated vasoconstriction. Additionally, we will look downstream of Rho-kinase, introducing a potential role for various substrates in the mechanism of Rho-kinase-mediated constriction in the cavernosal vasculature.

Publication types

  • Review

MeSH terms

  • Animals
  • Enzyme Activation / physiology
  • Humans
  • Intracellular Signaling Peptides and Proteins
  • Male
  • Muscle, Smooth / enzymology*
  • Penile Erection / physiology*
  • Penis / enzymology*
  • Protein-Serine-Threonine Kinases / physiology*
  • rho-Associated Kinases

Substances

  • Intracellular Signaling Peptides and Proteins
  • Protein-Serine-Threonine Kinases
  • rho-Associated Kinases