Changes in fibrinolytic activity after angiotensin II receptor blockade in therapy‐resistant hypertensive patients

Summary. 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 μg 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. Conclusion: Therapy-resistant hypertensive patients show beneficial changes in fibrinolytic activity after infusion of a non-pressor dose of AT1RB.