The responsiveness of platelets only to epinephrine was markedly impai
red in 23/140 (16%) healthy Japanese. The impaired responsiveness was
not altered by changes in time and environment. Circulating level of c
atecholamines did not affect the responsiveness of platelets to epinep
hrine. A pilot family study indicated a possible familial nature of th
e defect. H-3 methyl yohimbine binding studies indicated that this def
ect was due to the decreased number of alpha 2 adrenergic receptor. De
spite the defect, the potentiating effect of epinephrine on platelet a
ggregation stimulated by a low dose of ADP was normal. This abnormalit
y is not apparently associated with any bleeding disorders and the cli
nical implication is unknown at present. It is, however, essential to
acknowledge the prevalence of such defect in pursuing research on plat
elets stimulated by epinephrine.