Thromb Haemost 1996; 75(04): 635-641
DOI: 10.1055/s-0038-1650335
Original Article
Schattauer GmbH Stuttgart

High Density Lipoproteins Enhance the Na+/H+ Antiport in Human Platelets

Jerzy-Roch Nofer
1   The Institut für Klinische Chemie und Laboratoriumsmedizin, Zentrallaboratorium, Münster, Germany
,
Martin Tepel
2   Medizinische Poliklinik, Westfälische Wilhelms-Universitat, Münster, Germany
,
Beate Kehrel
3   Experimented Hämostaseforschung, Medizinische Klinik und Poliklinik, Innere Medizin A, Münster, Münster, Germany
,
Michael Walter
1   The Institut für Klinische Chemie und Laboratoriumsmedizin, Zentrallaboratorium, Münster, Germany
4   Institut für Arterioskleroseforschung an der Universität Münster, Münster, Germany
,
Udo Seedorf
4   Institut für Arterioskleroseforschung an der Universität Münster, Münster, Germany
,
Gerd Assmann
1   The Institut für Klinische Chemie und Laboratoriumsmedizin, Zentrallaboratorium, Münster, Germany
4   Institut für Arterioskleroseforschung an der Universität Münster, Münster, Germany
,
Walter Zidek
2   Medizinische Poliklinik, Westfälische Wilhelms-Universitat, Münster, Germany
› Author Affiliations
Further Information

Publication History

Received 28 September 1995

Accepted after revision 12 January 1996

Publication Date:
10 July 2018 (online)

Summary

In the present study, we investigated the effect of high density lipoproteins 3 (HDL3) on Na+/H+ exchanger activity and cytosolic pH (pHi) in human platelets. HDL3 alone failed to affect pHi? but preincubation with HDL3 significantly enhanced the Na+/H+ antiport activation brought about by acidification with 100 mM sodium propionate or stimulation with 0.05 U/ml thrombin. The stimulatory effect of HDL3 was unaffected by indomethacin excluding a role for cyclooxygenase products. The HDL3 effect was not mediated by Ca2+/calmodulin-dependent protein kinase as HDL3 failed to increase cytosolic free calcium concentration. However, the potentiating effect of HDL3 was completely blocked in the presence of the protein kinase C inhibitor, bisindoylmaleimide and the phosphatidylcholine-specific phospholi-pase C inhibitor, D609. Furthermore, the effect of HDL3 was abolished after covalent modification of HDL3 with dimethylsuberimidate and was not observed in platelets from Glanzmann thrombasthenia type 1 which do not express GP IIb/IIIa, as well as in platelets preincubated with anti-GP Ilb/IIIa polyclonal antibodies. We conclude that HDL3 enhances the sodium propionate- and thrombin-induced Na+/H+ antiport activity in human platelets via binding to GP Ilb/IIIa and activation of protein kinase C and phosphatidylcholine-specific phospholipase C.

 
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