title: Evidence of dysfunctional beta2-adrenoceptor signal system in pre-eclampsia.
abstract: OBJECTIVE
  To determine how beta2-adrenoceptor binding and function differ between healthy women and those with pre-eclampsia.
  
  
  METHODS
  Case-control study.
  
  
  METHODS
  Faculty of Medicine, University of Tromsø, Norway.
  
  
  METHODS
  Two groups of pregnant women: eight cases with pre-eclampsia, matched with eight healthy controls.
  
  
  METHODS
  Venous blood was drawn from women in both groups after an overnight rest. The two groups were matched for gestational age which was (mean (SD)) 36 x 4 (3 x 8) and 36 x 5 (4 x 4) weeks for the pre-eclamptic and control groups, respectively. Six weeks after delivery a second blood sample was obtained. The binding and function of beta2-adrenoceptors were determined in isolated human mononuclear leukocytes. The levels of adrenaline and noradrenaline were determined in plasma from venous blood.
  
  
  RESULTS
  An elevated density of functional beta2-adrenoceptors was observed in normal pregnancy [mean (SD) 390 (90) vs 270 (60) sites/cell postpartum], due to an increased fraction of receptors in high affinity state, with unaltered total receptor density. The number of functional beta2-adrenoceptors was reduced in pre-eclampsia [mean (SD) 80 (40) vs 240 (30) sites/cell postpartum], due to a reduction in the total receptor number with an unaltered fraction of high affinity receptors. In pregnancy, both unstimulated and isoprenaline-stimulated cAMP levels were reduced in the women with pre-eclampsia (0 x 5 (0 x 2) and 1 x 7 (0 x 9) pmol/10(6) cells, respectively) compared with the normal pregnant controls (mean (SD) 1 x 2 (0 x 3) and 4 x 7 (1 x 8) pmol/10(6) cells, respectively). Plasma catecholamine levels were not elevated in the women with pre-eclampsia.
  
  
  CONCLUSIONS
  The increased number of functional beta2-adrenoceptors may contribute to the vasodilatation seen in normal pregnancy, while the reduced overall number of receptors may be one of several factors that account for increased peripheral vascular resistance in pre-eclampsia.
authors.affiliation: Department of Obstetrics and Gynaecology, Institute of Clinical Medicine, University of Tromsø, Norway.
authors.forename: B
authors.initials: B
authors.lastname: Aune
authors.forename: A
authors.initials: A
authors.lastname: Vårtun
authors.forename: P
authors.initials: P
authors.lastname: Oian
authors.forename: G
authors.initials: G
authors.lastname: Sager
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000378:metabolism; D000328:Adult; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D020120:Iodocyanopindolol / Q000378:metabolism; D007545:Isoproterenol / Q000494:pharmacology; D011225:Pre-Eclampsia / Q000378:metabolism*; D011247:Pregnancy; D018343:Receptors, Adrenergic, beta-2 / Q000378:metabolism*
chemical_list: D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D018343:Receptors, Adrenergic, beta-2; D020120:Iodocyanopindolol; D007545:Isoproterenol