Depressed Responsiveness to Adrenaline in Platelets from Apparently Normal Human Donors: a Familial Trait
Article first published online: 12 MAR 2008
British Journal of Haematology
Volume 49, Issue 2, pages 303–314, October 1981
How to Cite
Scrutton, M. C., Clare, K. A., Hutton, R. A. and Bruckdorfer, K. R. (1981), Depressed Responsiveness to Adrenaline in Platelets from Apparently Normal Human Donors: a Familial Trait. British Journal of Haematology, 49: 303–314. doi: 10.1111/j.1365-2141.1981.tb07227.x
- Issue published online: 12 MAR 2008
- Article first published online: 12 MAR 2008
- Received 25 February 1981 accepted for publication 21 May 1981
Summary. Decreased responsiveness to adrenaline has been observed in five apparently normal unrelated human donors. In four 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 two 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°C or by addition of a low concentration of the divalent cation ionophore, A-23187. All affected platelets which have been examined have ATP and ADP contents, cholesterol to phospholipid ratios, and phospholipid class compositions within the normal range. Both the resting level of cyclic-3′,5′-AMP and the ability of adrenaline to prevent elevation of cyclic-3′.5′-AMP levels by prostaglandin E1 are normal. Mixing experiments demonstrate the absence of a circulating inhibitor of platelet function and suggest that the defect resides in the platelets. We conclude that the depressed responsiveness of human platelets to adrenaline may result from a defect in Ca2+ mobilization to the cytosol.