Thromb Haemost 1990; 64(04): 594-599
DOI: 10.1055/s-0038-1647364
Original Article
Schattauer GmbH Stuttgart

Hypersensitivity to Thromboxane A2 in Cholesterol-Rich Human Platelets

Takuya Tomizuka
The 2nd Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan
,
Kyohei Yamamoto
The 2nd Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan
,
Aizan Hirai
The 2nd Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan
,
Yasushi Tamura
The 2nd Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan
,
Sho Yoshida
The 2nd Department of Internal Medicine, School of Medicine, Chiba University, Chiba, Japan
› Author Affiliations
Further Information

Publication History

Received 12 February 1990

Accepted after revision23 July 1990

Publication Date:
25 July 2018 (online)

Summary

The effect of changes in platelet membrane cholesterol content on thromboxane A2 (TXA2)-induced platelet activation was studied. Concentrations of 9,ll-epithio-ll,12-methano-TXA2 (STA2), a stable analogue of TXA2 which can cause half-maximal aggregation and release of [14C]serotonin in cholesterol-rich platelets were significantly lower than those in cholesterol-normal platelets. STA2-induced increase in cytosolic calcium concentration and [32P]phosphatidic acid formation in cholesterol-rich platelets were significantly greater than those in cholesterol-normal platelets. The maximal concentration of binding site (Bmax) for SQ29548 was significantly increased in cholesterol-rich platelets compared with cholesterol-normal platelets, while the equilibrium dissociation rate constant (Kd) for SQ29548 did not differ between cholesterol-rich and cholesterol-normal platelets. The present study suggested that sensitivity to TXA2 was increased by the incorporation of cholesterol into platelet membrane and that the cause of hypersensitivity to TXA2 in cholesterol-rich platelets may be partly explained by an increase in binding capacity for TXA2.

 
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