title: The effect of angiotensin II on platelet intracellular free calcium concentration in human pregnancy.
abstract: OBJECTIVE
  The primary objective of this study was to determine the effect of i.v. angiotensin II infusion on platelet intracellular free calcium concentration in potentially hypertensive primigravid women.
  
  
  METHODS
  Patients at 28-32 weeks gestation were selected on the basis of a diastolic pressure less than or equal to 80 mmHg taken at the antenatal clinic visit.
  
  
  METHODS
  An angiotensin II infusion test (4-16 ng/kg per min) was performed in 13 women. Platelet intracellular free calcium concentration, platelet angiotensin II binding site density and plasma angiotensin II concentration were measured before and at the end of the infusion. Pregnancy outcome (normotension or hypertension) was recorded.
  
  
  RESULTS
  Platelet intracellular free calcium concentration rose in 12 of 13 women during angiotensin II infusion. This rise was not directly correlated with initial or final platelet angiotensin II binding site density, plasma angiotensin II concentration or the evoked change in systolic or diastolic blood pressure. Five women subsequently developed pregnancy-induced hypertension. Although basal platelet intracellular free calcium concentration did not differ between the two groups, platelet intracellular free calcium concentration rose twice as much in response to angiotensin II in the five hypertensive pregnant women. There was a 12-fold increase in platelet angiotensin II binding in the future hypertensives, although basal angiotensin II was the same in the two groups.
  
  
  CONCLUSIONS
  The enhanced rise in platelet intracellular free calcium concentration in response to angiotensin II administration in women who subsequently became hypertensive, together with their increased angiotensin II binding site density suggest a possible enhanced stimulus-effect coupling. Pregnancy-induced hypertension is a state of marked vasoconstriction, with an enhanced pressor response to angiotensin II. These data supply grounds for a hypothesis concerning the mechanism.
authors.affiliation: Department of Obstetrics and Gynaecology, University Hospital, Nottingham, UK.
authors.forename: P N
authors.initials: PN
authors.lastname: Baker
authors.forename: M D
authors.initials: MD
authors.lastname: Kilby
authors.forename: F
authors.initials: F
authors.lastname: Broughton Pipkin
mesh_terms: D000328:Adult; D000804:Angiotensin II / Q000494:pharmacology*; D001792:Blood Platelets / Q000187:drug effects*; D001794:Blood Pressure / Q000502:physiology; D002118:Calcium / Q000097:blood*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000453:epidemiology; D011247:Pregnancy / Q000097:blood*; D011249:Pregnancy Complications, Cardiovascular / Q000097:blood* / Q000453:epidemiology; D011256:Pregnancy Outcome; D011446:Prospective Studies; D015290:Second Messenger Systems / Q000502:physiology
chemical_list: D000804:Angiotensin II; D002118:Calcium