title: Angiotensin II sensitivity in nonpregnant formerly preeclamptic women and healthy parous controls.
abstract: BACKGROUND
  In women prone to develop hypertensive complications, vascular reactivity fails to decrease in early pregnancy. Since hypertensive syndromes of pregnancy seem to be superimposed on a preexisting disorder, we tested the hypothesis that in formerly preeclamptic women, as compared to healthy parous controls, circulatory reactivity to angiotensin II is enhanced in the follicular phase of the menstrual cycle.
  
  
  METHODS
  Sixty formerly preeclamptic women were subdivided into a hypertensive (HYPERT, n = 14), a normotensive thrombophilic (THROMB, n = 26), and a normotensive nonthrombophilic (ASYMPT, n = 20) subgroup. In these women and in 11 healthy parous controls we assessed at least 5 months postpartum at day 5 (+/-2) of the menstrual cycle the following variables: body weight, height, plasma volume, reactivity to infused angiotensin II of arterial blood pressure, heart rate, glomerular filtration rate (GFR), effective renal blood flow, and the hormones of the renin-angiotensin-aldosterone (RAAS) axis.
  
  
  RESULTS
  At baseline, THROMB did not differ from controls. In contrast, ASYMPT exhibited slight overweight, reduced plasma volume, and reduced renal blood flow. HYPERT much resembled ASYMPT except for the overweight, renal perfusion, and GFR. Infusion of angiotensin II led to comparable decreases in renal perfusion and filtration, and to increases in blood pressure. However, sensitivity to this substance correlated inversely with relative and absolute sizes of the plasma volume compartment.
  
  
  CONCLUSIONS
  Circulatory sensitivity to infused angiotensin II is comparable between nonpregnant formerly preeclamptic women and healthy parous controls. However, responsiveness to this agent is enhanced among women with a contracted plasma volume compartment, a condition commonly observed among formerly preeclamptic women.
authors.affiliation: Department of Obstetrics & Gynecology, Maastricht, The Netherlands. marc.spaanderman@og.unimaas.nl
authors.forename: Marc E A
authors.initials: ME
authors.lastname: Spaanderman
authors.forename: Timo H A
authors.initials: TH
authors.lastname: Ekhart
authors.forename: Peter W
authors.initials: PW
authors.lastname: de Leeuw
authors.forename: Louis L H
authors.initials: LL
authors.lastname: Peeters
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000494:pharmacology*; D001794:Blood Pressure; D001835:Body Weight; D005260:Female; D005498:Follicular Phase / Q000502:physiology*; D006339:Heart Rate; D006801:Humans; D046110:Hypertension, Pregnancy-Induced / Q000503:physiopathology* / Q000517:prevention & control*; D007668:Kidney / Q000098:blood supply; D010298:Parity; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D012039:Regional Blood Flow; D012307:Risk Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology*
chemical_list: D014662:Vasoconstrictor Agents; D000804:Angiotensin II