BACKGROUND/AIMS: Angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists have beneficial effects on impaired fibrinolytic activity of hypertensive patients. The aim of the study was to evaluate the effect of antialdosterone treatment on impaired fibrinolysis of hypertensive patients. METHODS: Fourteen hypertensive outpatients and 14 normotensive healthy volunteers participated in this study. Blood samples for plasminogen activator inhibitor-1 (PAI-1) antigen and tissue plasminogen activator (t-PA) antigen were obtained at baseline in all patients and control subjects. Then all hypertensive patients used spironolactone 50 mg/day for a week. Blood samples were again obtained after a week of spironolactone treatment. RESULTS: The mean basal plasma level of PAI-1 of hypertensive patients was higher than those of the normotensive control group (60.98 +/- 4.2 vs. 24.09 +/- 1.61 ng/ml, p < 0.01) The mean basal t-PA level was similar in the hypertensive and control subjects (7.49 +/- 0.65 vs. 8.78 +/- 0.92 ng/ml, p > 0.05). The mean PAI-1 level decreased after a week of spironolactone treatment (60.98 +/- 4.2 vs. 42.99 +/- 7.98 ng/ml, p < 0.05). The mean plasma t-PA level of hypertensive patients increased after spironolactone treatment (7.49 +/- 0.65 vs. 11.09 +/- 1.33 ng/ml, p < 0.05). CONCLUSION: This study shows that spironolactone improves impaired fibrinolysis in systemic hypertension. It provides evidence for a direct link between aldosterone and the fibrinolytic system in humans. Copyright 2002 S. Karger AG, Basel
BACKGROUND/AIMS: Angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists have beneficial effects on impaired fibrinolytic activity of hypertensivepatients. The aim of the study was to evaluate the effect of antialdosterone treatment on impaired fibrinolysis of hypertensivepatients. METHODS: Fourteen hypertensive outpatients and 14 normotensive healthy volunteers participated in this study. Blood samples for plasminogen activator inhibitor-1 (PAI-1) antigen and tissue plasminogen activator (t-PA) antigen were obtained at baseline in all patients and control subjects. Then all hypertensivepatients used spironolactone 50 mg/day for a week. Blood samples were again obtained after a week of spironolactone treatment. RESULTS: The mean basal plasma level of PAI-1 of hypertensivepatients was higher than those of the normotensive control group (60.98 +/- 4.2 vs. 24.09 +/- 1.61 ng/ml, p < 0.01) The mean basal t-PA level was similar in the hypertensive and control subjects (7.49 +/- 0.65 vs. 8.78 +/- 0.92 ng/ml, p > 0.05). The mean PAI-1 level decreased after a week of spironolactone treatment (60.98 +/- 4.2 vs. 42.99 +/- 7.98 ng/ml, p < 0.05). The mean plasma t-PA level of hypertensivepatients increased after spironolactone treatment (7.49 +/- 0.65 vs. 11.09 +/- 1.33 ng/ml, p < 0.05). CONCLUSION: This study shows that spironolactone improves impaired fibrinolysis in systemic hypertension. It provides evidence for a direct link between aldosterone and the fibrinolytic system in humans. Copyright 2002 S. Karger AG, Basel