title: Changes in fibrinolytic activity after angiotensin II receptor blockade in therapy-resistant hypertensive patients.
abstract: BACKGROUND
  In hypertensive patients, the activated renin-angiotensin system induces a prothrombotic state resulting from imbalance between coagulation and fibrinolysis. Although blood pressure cannot be regulated in therapy-resistant hypertensive patients, they may still be responsive to medication that attenuates the renin-angiotensin system.
  
  
  OBJECTIVE
  our objective was to study possible attenuating properties of angiotensin II type 1 receptor blockers (AT1RBs) on the prothrombotic state in therapy-resistant hypertensive patients, focusing on parameters of fibrinolysis and coagulation.
  
  
  METHODS
  Fourteen therapy-resistant hypertensive patients received AT1RB eprosartan infusion (45 and 150 microg kg(-1)) (study group), and 33 therapy-resistant hypertensive patients received saline (0.9%) infusion (control group) prior to renal angiography. Baseline values of parameters of coagulation and fibrinolysis were set at 1.00, and relative changes were calculated.
  
  
  RESULTS
  Plasminogen activator inhibitor type 1 (PAI-1) antigen showed non-significant decreases in both the study group (arterial 1.00-0.45, venous 1.00-0.42) and control group (arterial 1.00-0.84, venous 1.00-0.88). PAI-1 activity significantly decreased in the study group (arterial 1.00-0.72, venous 1.00-0.71) and control group (arterial 1.00-0.83, venous 1.00-0.94). In the study group, tissue-type plasminogen activator (t-PA) antigen decreased significantly (arterial 1.00-0.62, venous 1.00-0.67), whereas t-PA activity significantly increased (arterial 1.00-6.15, venous 1.00-2.66). In the control group, t-PA antigen remained unchanged. No changes were observed in blood pressure during and after infusion of eprosartan.
  
  
  CONCLUSIONS
  Therapy-resistant hypertensive patients show beneficial changes in fibrinolytic activity after infusion of a non-pressor dose of AT1RB.
authors.affiliation: Laboratory for Clinical Thrombosis and Haemostasis, Department of Internal Medicine, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
authors.forename: A W J H
authors.initials: AW
authors.lastname: Dielis
authors.forename: M
authors.initials: M
authors.lastname: Smid
authors.forename: H M H
authors.initials: HM
authors.lastname: Spronk
authors.forename: A J H M
authors.initials: AJ
authors.lastname: Houben
authors.forename: K
authors.initials: K
authors.lastname: Hamulyák
authors.forename: A A
authors.initials: AA
authors.lastname: Kroon
authors.forename: H
authors.initials: H
authors.lastname: Ten Cate
authors.forename: P W
authors.initials: PW
authors.lastname: de Leeuw
mesh_terms: D000179:Acrylates / Q000494:pharmacology; D000328:Adult; D000368:Aged; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology*; D001777:Blood Coagulation / Q000187:drug effects; D016022:Case-Control Studies; D004351:Drug Resistance; D042783:Endothelial Cells / Q000187:drug effects; D005260:Female; D005342:Fibrinolysis / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000188:drug therapy*; D007093:Imidazoles / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D013876:Thiophenes / Q000494:pharmacology
chemical_list: D000179:Acrylates; D047228:Angiotensin II Type 1 Receptor Blockers; D007093:Imidazoles; D013876:Thiophenes; C068373:eprosartan