I006: Effects of the mineralocorticoid fludrocortisone on fibrinolytic function in normal subjects

• Published in: American journal of hypertension Vol. 13; no. S2; pp. 176A - 177A
• Main Authors: Lottermoser, K., Hertfelder, H.H., Schiermeyer, B., Vetter, H., Düsing, R.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.04.2000
• Subjects: fibrinolytic function; Fludrocortisone; plasminogen activator inhibitor 1; tissue plasminogen activator
• ISSN: 0895-7061; 1941-7225; 1879-1905
• DOI: 10.1016/S0895-7061(00)01153-5

Accumulating evidence suggests that the renin-angiotensin aldosterone system (RAAS) may participate in the regulation of fibrinolytic function. Angiotensin II is the primary candidate to mediate this interrelationship since angiotensin II is capable to stimulate PAI-1 in vitro and in-vivo. It has been suggested that aldosterone may also modulate fibrinolysis possibly by interacting with angiotensin II. The present study therefore investigates the effect of short-term treatment with the synthetic mineralocorticoid fludrocortisone (F) on fibrinolytic function. 10 healthy male volunteers aged 25–30 years on a constant intake of 160–180 mmol Na+ and 60–80 mmol K+ were studied on a control day (C1), after 2 days of oral administration of F (0.1 mg bid), and again 5 days after F (C2). F was associated with a marked decrease in plasma renin activity (PRA) from 0.88 ± 0.49 ng ml−1 h−1 to 0.35 ± 0.32 ng ml−1 h−1 (p < 0.001), which returned to the baseline range at C2 (0.64 ± 0.41 ng ml−1 h−1). The experimental protocol was not associated with changes in the activity or antigen concentration of tissue plasminogen activator (t-PA). PAI-1 exhibited a circadian rhythm with highest values at 08.00 AM (41.8 ± 9.5 ng/ml) decreasing to 12.30 AM (22.6 ± 5.8 ng/ml) and 04.30 PM (12.3 ± 3.3 ng/ml). At all three time points, PAI-1 was unchanged by the mineralocorticoid. Our results therefore do not support a major mineralocorticoid effect on PAI-1. However, our study does not exclude a modulatory role of F since unchanged PAI-1 could be observed in spite of a marked suppression of the renin-angiotensin system.