Several lines of evidence point to an interrelation of the renin-angiotensin system
(RAS) with the endogenous fibrinolytic system. 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. 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. In conclusion, this study 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 inhibition exerts vasculo protective effects and
reduces the risk of atherothrombotic events.

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