Abstract
Background: Several lines of evidence point to an interrelation of the renin angiotensin system (RAS) with the endogenous fibrinolytic system. Aim & Methods: this study was planned to examine the effect of salt depletion as a method of activation of the endogenous RAS on plasma fibrinolytic balance in 10 healthy human subjects in the presence and absence of Angiotensin converting enzyme inhibitor- ACEi (captopril). Activation of the RAS during low salt intake was documented by a significant increase in serum aldosterone concentration. Results: the data suggest that activation of the RAS results in increased plasminogen activator inhibitors (PAI-I) antigen and that interruption of the RAS with the ACE inhibitor captopril significantly lowers PAI-I antigen without lowering tissue-type plasminogen activator (t-PA) antigen. Conclusion: this data provides an evidence of a direct functional link between the RAS and the fibrinolytic system in humans and these findings may help to elucidate possible mechanisms by which ACE inhibitionexerts vasculoprotective effects and reduces the risk of atherothrombotic events.
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