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Published on: April 1, 2015
Fibrinolytic function in diuretic-induced volume depletion
K Lottermoser1, H J Hertfelder, H Vetter
1Medizinische Universitäts-Poliklinik and Institut für Experimentelle Hämatologie und Transfusionsmedizin, Bonn, Germany.
American Journal of Hypertension
|May 23, 2000
Summary
Hydrochlorothiazide (HCT) increases plasminogen activator inhibitor-1 (PAI-1), a key regulator of fibrinolysis. Losartan, an angiotensin II receptor antagonist, blunts this HCT-induced rise in PAI-1, suggesting the angiotensin II type 1 receptor
Area of Science:
- Cardiovascular Physiology
- Hemostasis and Thrombosis
- Endocrinology
Background:
- The renin-angiotensin system (RAS) is implicated in regulating fibrinolysis.
- Previous studies with ACE inhibitors and losartan showed inconsistent effects on endogenous fibrinolysis.
- The impact of RAS modulation on fibrinolysis may depend on the degree of system prestimulation.
Purpose of the Study:
- To investigate the effects of hydrochlorothiazide (HCT) and losartan on fibrinolytic function.
- To determine if angiotensin II receptor blockade can modulate HCT-induced changes in fibrinolysis.
- To explore the role of the RAS in regulating plasminogen activator inhibitor-1 (PAI-1).
Main Methods:
- 15 healthy volunteers participated in a 12-day study.
- Fibrinolytic parameters were assessed at baseline, after 10 days of HCT treatment, and after acute losartan administration.
- Plasma renin activity (PRA), tissue-type plasminogen activator (t-PA), and PAI-1 antigen and activity were measured.
Main Results:
- HCT treatment significantly increased plasma renin activity (PRA) and plasminogen activator inhibitor-1 (PAI-1) antigen levels.
- HCT treatment also showed a trend towards increasing PAI-1 activity.
- Acute losartan administration further increased PRA but blunted the HCT-induced rise in PAI-1 antigen and activity.
Conclusions:
- Volume depletion induced by HCT is associated with increased PAI-1 levels.
- Acute blockade of the angiotensin II type 1 receptor with losartan can attenuate the rise in PAI-1.
- These findings suggest that the angiotensin II type 1 receptor plays a role in mediating the effects of angiotensin II on PAI-1 during volume depletion.
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