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Thrombin‐induced platelet aggregation is affected by external Na + independently of the Na + /H + exchange
Author(s) -
Agam G.,
Argaman A.,
Livne A.
Publication year - 1989
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(89)81199-8
Subject(s) - thrombin , chemistry , sphingosine , platelet activation , amiloride , platelet , platelet aggregation , biophysics , biochemistry , sodium , receptor , medicine , biology , organic chemistry
Thrombin affects blood platelets by activation of Na + /H + exchange and induction of aggregation, but the relationship between these effects is under debate. The present study attempts to clarify whether the activation of the exchanger activity is required for platelet aggregation. In apparent support of such a requirement, thrombin‐induced aggregation is higher in Na + medium than in N ‐methylglucamine + medium and is inhibited by sphingosine, an inhibitor of protein kinase C known to regulate the Na + /H + exchanger. However, the inhibition of aggregation by sphingosine occurs in both Na + ‐containing and Na + ‐free media, the aggregation is identical in Na + and K + ‐containing media, and is not inhibited by 5‐ N ‐(3‐aminophenyl)amiloride, at a concentration 10‐fold higher than its K i for platelet Na + /H + exchange. Furthermore, at low concentration (0.005 U/ml) thrombin induces aggregation but does not activate the exchange. It is concluded that the activation of Na + /H + exchange is not required for thrombin‐induced platelet aggregation and that the apparent augmentation of aggregation by Na + is due to an inhibitory effect of N ‐methylglucamine + .