Lack of vasopressin-induced platelet aggregation in healthy subjects

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  • Urakami Masaya
    Second Department of Internal Medicine, Kansai Medical University
  • Umeda Yukihisa
    Second Department of Internal Medicine, Kansai Medical University
  • Yamane Yoko
    Second Department of Internal Medicine, Kansai Medical University

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We found 3 subjects whose platelets lacked an aggregation response to arginine vasopressin (AVP) out of 36 healthy subjects. These 3 subjects (Non-Responders; NR) were compared with 8 subjects whose platelets responded completely to AVP (Responders; R). All cases were young healthy men without bleeding disorders or tendencies. Platelet function was evaluated by aggregation response to AVP, adenosine diphosphate (ADP), collagen, and epinephrine. Resting and AVP-stimulated [Ca2+]i in platelets were also measured. We measured AVP levels in platelet free plasma (PFP) and in platelets, and characterized AVP receptor on platelets. There were no significant differences in platelet aggregation with ADP, collagen, and epinephrine between the 2 groups. Addition of AVP to platelets showed a rapid but transient increase in [Ca2+]i in both groups, but the peak level was extremely low in NR. The binding experiment demonstrated that maximal binding capacity (B max) of AVP receptor on platelets was significantly reduced in NR (B max; 213 ± 12 SEM sites/cell in N vs.30 ± 4 sites/cell in NR). PFP and platelet AVP levels did not differ between the 2 groups. These results indicate that the selective lack of platelet aggregation with AVP is caused probably by congenitally reduced B max of AVP receptor.

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