title: Angiotensin II increases corpus cavernosal contractility and oxidative stress in partial bladder outlet obstructed rabbits: relevance to erectile dysfunction.
abstract: BACKGROUND
  We investigated the effect angiotensin II (Ang II), a corpus cavernosal smooth muscle (CCSM) constrictor peptide, has on tissue taken from rabbits following chronic partial bladder outlet obstruction (PBOO), as this model is characterized by an increase in corpus cavernosal collagen deposition and a marked reduction and impaired relaxation of CCSM cells.
  
  
  OBJECTIVE
  To determine the interaction between Ang II and nitric oxide (NO) and the development of oxidative stress (OS) in a rabbit model of chronic PBOO.
  
  
  METHODS
  Corpus cavernosal tissue was obtained from 12 sham-operated and 20 PBOO rabbits. Organ bath studies determined Ang II/NO interaction on CCSM function using losartan (AT1 receptor antagonist), sodium nitroprusside (SNP, NO donor), electrical field stimulation (EFS), and vardenafil (phosphodiesterase type 5 inhibitor). The role of OS in the Ang II response was also determined using diphenylene iodonium chloride (DPI), the nicotinamide adenine dinucleotide phosphate oxidase inhibitor, which inhibits superoxide production and superoxide dismutase (SOD, the enzyme that accelerates the breakdown of superoxide).
  
  
  METHODS
  Action of Ang II and AT1 receptor antagonist, as well as SOD and DPI on CCSM function.
  
  
  RESULTS
  Ang II caused a dose-dependent contraction of CCSM strips that was enhanced in PBOO rabbits and inhibited by losartan, DPI, and SOD. CCSM relaxation induced by SNP/EFS was impaired in this model and improved by vardenafil and losartan.
  
  
  CONCLUSIONS
  These findings imply that the increased Ang II contractile response is a pathological consequence of PBOO and that AT1 receptor inhibition may be a therapeutic approach to treat ED associated with PBOO.
authors.affiliation: Department of General Surgery, Division of Interventional Science, University College London Medical School, London, UK.
authors.forename: Hani
authors.initials: H
authors.lastname: Ertemi
authors.forename: David H W
authors.initials: DH
authors.lastname: Lau
authors.forename: Dimitri P
authors.initials: DP
authors.lastname: Mikhailidis
authors.forename: Faiz H
authors.initials: FH
authors.lastname: Mumtaz
authors.forename: Cecil S
authors.initials: CS
authors.lastname: Thompson
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology / Q000502:physiology*; D000818:Animals; D004195:Disease Models, Animal; D004558:Electric Stimulation; D007172:Erectile Dysfunction / Q000378:metabolism / Q000503:physiopathology*; D007093:Imidazoles / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009126:Muscle Relaxation / Q000187:drug effects; D009130:Muscle, Smooth / Q000187:drug effects / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D020030:Nitric Oxide Donors / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D018384:Oxidative Stress; D010413:Penis / Q000187:drug effects / Q000502:physiology*; D058986:Phosphodiesterase 5 Inhibitors / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology; D011817:Rabbits; D013450:Sulfones / Q000494:pharmacology; D014227:Triazines / Q000494:pharmacology; D001748:Urinary Bladder Neck Obstruction / Q000503:physiopathology; D000069058:Vardenafil Dihydrochloride
chemical_list: D007093:Imidazoles; D020030:Nitric Oxide Donors; D058986:Phosphodiesterase 5 Inhibitors; D010879:Piperazines; D013450:Sulfones; D014227:Triazines; D000804:Angiotensin II; D009599:Nitroprusside; D009569:Nitric Oxide; D000069058:Vardenafil Dihydrochloride