Depressed Responsiveness to Adrenaline in Platelets from Apparently Normal Human Donors: a Familial Trait

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Abstract
Decreased responsiveness to adrenaline [epinephrine] was observed in 5 apparently normal unrelated human donors. In 4 of the donors this trait is inherited. Three of the donors, as well as their affected relatives, also exhibit depressed responsiveness to collagen and vasopressin but normal responsiveness to ADP and thrombin. The other 2 affected donors exhibit normal responsiveness to most other agonists. Normal responsiveness can be restored in all instances either by incubating the platelet-rich plasma at 20.degree. C or by addition of a low concentration of the divalent cation ionophore, A-23187. All affected platelets examined have ATP and ADP contents, cholesterol to phospholipid ratios, and phospholipid class compositions within the normal range. Both the resting level of cAMP and the ability of adrenaline to prevent elevation of cAMP levels by prostaglandin E1 are normal. The absence of a circulating inhibitor of platelet function suggests that the defect resides in the platelets. The depressed responsiveness of human platelets to adrenaline may result from a defect in Ca2+ mobilization to the cytosol.