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Journal Article

Stimulation of human platelets by collagen occurs by a Na+/H+ exchanger independent mechanism


Siffert,  Winfried
Department of Physiology, Max Planck Institute of Biophysics, Max Planck Society;

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Joseph, S., Siffert, W., Gorter, G., & Akkerman, J.-W.-N. (1990). Stimulation of human platelets by collagen occurs by a Na+/H+ exchanger independent mechanism. Biochimica et Biophysica Acta-Molecular Cell Research, 1054(1), 26-32. doi:10.1016/0167-4889(90)90201-n.

Cite as: https://hdl.handle.net/21.11116/0000-0007-F59C-5
In stimulated human platelets dense-granule secretion in response to the 'weak agonists' ADP, adrenaline, platelet activating factor and low concentrations of thrombin as well as Ca2+ mobilisation in response to thrombin are enhanced by a Na+/H+ exchanger. In the present study the role of this antiport in collagen stimulated human platelets was examined. While stimulation of platelets loaded with the fluorescent intracellular pH-sensitive dye, bis-carboxyethyl-5-(6)-carboxyfluorescein (BCECF) with thrombin resulted in the activation of the Na+/H+ exchanger, activation of this antiport did not occur in collagen-stimulated platelets. The lack of antiport activity in response to collagen using BCECF-loaded platelets correlated with the lack of any functional role of the antiport in collagen stimulated platelets. In the presence of a Na+/H+ exchange inhibitor, ethylisopropylamiloride, neither collagen-induced platelet aggregation or dense-granule secretion was affected. Furthermore, while the removal of extracellular Na+ (Na+ext), a condition that also prevents activation of the antiport, inhibited dense-granule secretion in response to a low concentration of thrombin, collagen-induced secretion was potentiated. This potentiatory effect could not be attributed to changes in either the membrane potential or in collagen-induced phospholipase C or protein kinase C activity. The present results indicate that in contrast to the 'weak agonists' (1) collagen-induced platelet activation does not require activation of the Na+/H+ exchanger and (2) Na+ext per se is an inhibitor of collagen-induced secretion.