The effect of antihypertensive drugs on protein adsorption, platelet adhesion, and blood coagulation toward an artificial surface.

Protein adsorption and platelet adhesion are two important biological processes arising at the blood-prosthetic interface. The ability of certain antihypertensive and anticholesterol drugs, namely, clonidine, hydralazine, sembrina, frusemide, clofibrate, sorbitrate, thyroxine, etc., to modulate the surface-induced platelet adhesion to polycarbonate substrate was investigated using washed calf platelets in the presence and absence of fibrinogen. This study also demonstrated the changes in protein-surface binding with these drugs using electrophoretic techniques. It seems that the addition of these drugs to the polymer-protein system increased the level of surface-bound albumin variably. These drugs also reduced the fibrinogen surface concentration and inhibited the surface-induced platelet adhesion to variable degrees. Therefore, it may be possible that the enhanced albumin-surface concentration, or reduced fibrinogen-surface binding, in the presence of these drugs may be one of the parameters for a reduced platelet-surface attachment, which may also improve the blood compatibility of the substrate. A better understanding of the mechanism of these drugs under in vivo conditions is needed to correlate these findings.