title: Phosphodiesterase-5 inhibitors and omental and placental small artery function in normal pregnancy and pre-eclampsia.
abstract: OBJECTIVE
  In pre-eclampsia (PE), endothelium-dependent function of myometrial small arteries is markedly attenuated. The residual PE response is wholly NO mediated. We have previously demonstrated that PDE5 inhibition can improve endothelial function in myometrial small arteries from women with PE. We aimed to assess whether the effect of PDE5 inhibition in PE was myometrial artery specific.
  
  
  METHODS
  Small arteries were dissected from omental biopsies obtained at Caesarean section from normal pregnant women (NP, N = 20) and women with PE (N = 11). Chorionic plate small arteries were dissected from NP (N = 13) and PE (N = 11) placentae. Vasoconstriction (arginine vasopressin or thromboxane-mimetic U46619) and endothelial-dependent relaxation were assessed by wire and pressure myography. Constriction/relaxation curves were repeated post 1h incubation with PDE5 inhibitors UK-343664 or sildenafil citrate (0, 10 or 100 nM).
  
  
  RESULTS
  Omental artery constriction was increased in PE. Omental vessel constriction was unaffected by PDE5 inhibition. Sildenafil citrate improved bradykinin-induced but not acetylcholine-induced relaxation of omental small arteries from NP women. PDE5 inhibition did not alter relaxation of omental arteries from women with PE. Placental small arteries were unaffected by PDE5 inhibition.
  
  
  CONCLUSIONS
  Use of PDE5 inhibitors does not significantly alter endothelial-dependent relaxation in omental or placental small arteries from PE women.
authors.affiliation: Maternal and Fetal Health Research Centre, St. Mary's Hospital, University of Manchester, Hathersage Road, Manchester M130JH, UK. mark.wareing@man.ac.uk
authors.forename: Mark
authors.initials: M
authors.lastname: Wareing
authors.forename: Jenny E
authors.initials: JE
authors.lastname: Myers
authors.forename: Maureen
authors.initials: M
authors.lastname: O'Hara
authors.forename: Louise C
authors.initials: LC
authors.lastname: Kenny
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Taggart
authors.forename: Laurence
authors.initials: L
authors.lastname: Skillern
authors.forename: Ian
authors.initials: I
authors.lastname: Machin
authors.forename: Philip N
authors.initials: PN
authors.lastname: Baker
mesh_terms: D000704:Analysis of Variance; D001160:Arterioles / Q000187:drug effects*; D001706:Biopsy; D016022:Case-Control Studies; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology; D005260:Female; D006801:Humans; D009213:Myography; D009215:Myometrium / Q000098:blood supply; D009852:Omentum / Q000098:blood supply*; D058986:Phosphodiesterase 5 Inhibitors; D010726:Phosphodiesterase Inhibitors / Q000008:administration & dosage / Q000494:pharmacology*; D010879:Piperazines / Q000494:pharmacology; D010920:Placenta / Q000098:blood supply*; D011225:Pre-Eclampsia / Q000188:drug therapy / Q000503:physiopathology*; D011247:Pregnancy / Q000502:physiology*; D011687:Purines / Q000494:pharmacology; D011744:Pyrimidinones / Q000494:pharmacology; D000068677:Sildenafil Citrate; D013450:Sulfones / Q000494:pharmacology; D016896:Treatment Outcome; D014590:Uterine Contraction; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D058986:Phosphodiesterase 5 Inhibitors; D010726:Phosphodiesterase Inhibitors; D010879:Piperazines; D011687:Purines; D011744:Pyrimidinones; D013450:Sulfones; C450961:UK 343,664; D014665:Vasodilator Agents; D000068677:Sildenafil Citrate