Abstract
The metabolism of inositol phospholipids in response to epinephrine was investigated in intact human platelets. In platelets prelabelled with [ 3H]-myo-inositol in Ca 2+-free HEPES buffer containing 10 mM LiCl, epinephrine caused an accumulation of inositol-1-phosphate in a concentration-dependent manner. The EC 50 value for epinephrine was 5 uM. Yohimbine (1 uM), a selective alpha-2 adrenergic receptor antagonist, inhibited 88% of the epinephrine (10 uM) response, whereas prazosin (1 uM), a selective alpha-1 adrenergic receptor antagonist, failed to inhibit the response. Yohimbine inhibited the epinephrine (10 uM) response in a concentration-dependent manner. The inhibition constant (Ki) value for yohimbine was 60.3 nM. These data indicate that epinephrine stimulates phosphoinositide (PI) turnover by activating adrenergic receptors of the alpha-2 type in human platelets. In addition, this PI response elicited by epinephrine was found to be inhibited in a concentration-dependent manner by treatment of platelets with dibutyryl cyclic AMP and 8-bromo-cyclic GMP which are knowm as potent inhibitors for platelet activation, and may therefore be a useful biochemical index for the study of the function of human alpha-2 adrenergic receptors.
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