Amphiphiles, known to induce exo- and endovesiculation in human erythrocytes, were studied by means of transmission electron microscopy (TEM) for their ability to induce shedding of vesicles (microparticles) from the porcine platelet plasma membrane. While echinocytogenic amphiphiles induced shedding of vesicles to the extracellular medium (exovesiculation), stomatocytogenic amphiphiles did not induce endovesiculation. The rapid (< 1 min) formation of many thin spicules in platelets upon treatment with echinocytogenic amphiphiles, indicates that spicule-formation is caused by a primary interaction of the amphiphile with the plasma membrane. Agonist- (Ca(2+)-ionophore A23187, thrombin and collagen) induced shape changes, however, seem to involve contractile cytoskeletal processes since treated cells attained heavily irregular shapes with broad pseudopods. Our study indicates that the mechanisms involved in amphiphile- and agonist-induced exovesiculation differ. Amphiphile-induced exovesicles are mainly electron-dense spherical structures (phi 150-200 nm) which originate from the formed spicules. Ionophore A23187-induced exovesicles are large (phi 200-800 nm) predominantly electron-lucent structures which are mainly shed from the cell body and seem to originate from extrusions of the canalicular system. Our study shows that there are several similarities but also obvious differences in the response of platelets and erythrocytes to amphiphile-treatment.