title: Rho kinase (ROK)-related proteins in human cavernous arteries: an immunohistochemical and functional approach.
abstract: BACKGROUND
  Rho kinases (ROKs) cause calcium-independent modulation of smooth muscle contraction. A significant role for the RhoA/ROK pathway in mediating the contraction of the penile erectile tissue has been suggested. Moreover, it has been postulated that ROK activity might represent a key factor in the pathophysiology of erectile dysfunction. Up until today, little is known on the significance of ROK and related proteins in the control of blood flow in the corpus cavernosum.
  
  
  OBJECTIVE
  To investigate by means of immunohistochemistry and organ bath studies the significance of the Rho pathway in human cavernous arteries.
  
  
  METHODS
  The expression of ROK1, ROK2, RhoA, and RhoGDI in human cavernous arteries was investigated by means of immunohistochemistry; myographic studies were conducted in order to characterize the effects of the ROK inhibitor Y27632 on isolated cavernous arteries.
  
  
  METHODS
  Specimens of human cavernous arteries were processed for immunohistochemistry for ROK1, ROK2, RhoA, and RhoGDI. Circular penile vascular segments were mounted in a tissue bath and the effects of increasing concentrations of the ROK inhibitor Y27632 on the tension induced by norepinephrine (NE, 1 µM) were investigated.
  
  
  RESULTS
  Alpha-actin immunoreactive cavernous arterioles also presented abundant staining specific for ROK1, ROK2, RhoA, and RhoGDI in the smooth musculature of the vascular wall. Cumulative addition of Y27632 dose-dependently reversed the tension induced by NE of isolated arterial segments. Y27632 produced relaxant responses with a reversion of tension of 34.3 ± 11.8% at a concentration of 1 µM.
  
  
  CONCLUSIONS
  The findings are in support for a role of the Rho/ROK-mediated signaling in the regulation of muscle tone of human cavernous arteries.
authors.affiliation: Hannover Medical School, Division of Surgery, Department of Urology & Urological Oncology, Hannover, Germany. sue_de_99@yahoo.de
authors.forename: Eginhard S
authors.initials: ES
authors.lastname: Waldkirch
authors.forename: Stefan
authors.initials: S
authors.lastname: Ückert
authors.forename: Michael
authors.initials: M
authors.lastname: Sohn
authors.forename: Markus A
authors.initials: MA
authors.lastname: Kuczyk
authors.forename: Petter
authors.initials: P
authors.lastname: Hedlund
mesh_terms: D000328:Adult; D000577:Amides / Q000494:pharmacology; D001158:Arteries / Q000201:enzymology / Q000502:physiology*; D004305:Dose-Response Relationship, Drug; D006801:Humans; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000201:enzymology / Q000502:physiology; D010413:Penis / Q000098:blood supply* / Q000201:enzymology / Q000502:physiology; D011725:Pyridines / Q000494:pharmacology; D015398:Signal Transduction / Q000502:physiology; D055815:Young Adult; D054460:rho-Associated Kinases / Q000037:antagonists & inhibitors / Q000502:physiology*
chemical_list: D000577:Amides; D011725:Pyridines; C108830:Y 27632; D054460:rho-Associated Kinases