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

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.