Abstract
In 1963 O’Brien was the first to document adrenaline induced aggregation in human platelets1. This functional response is not associated with the initial platelet shape change characteristic of the other agonists, and furthermore, full aggregation to adrenaline in vitro has only been observed for platelets obtained from some primates. Enhancement of aggregation by adrenaline to suboptimal concentrations of other agents (ie pro-aggregation) is seen in other animals as well as primates2, although the extent of even this response is quite variable amongst the species. Initial studies indicated that the adrenaline induced aggregatory response was mediated via an α-adrenoceptor on the platelet surface membrane, and in addition, the presence of β-adrenoceptors on mammalian platelets has been suggested by the anti-aggregatory effects of specific β-adrenergic agonist compounds3.
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Barnett, D.B., Swart, S.S., Nahorski, S.R., Cook, N. (1985). Characterisation of Human Platelet Adrenoceptors. In: Westwick, J., Scully, M.F., MacIntyre, D.E., Kakkar, V.V. (eds) Mechanisms of Stimulus—Response Coupling in Platelets. Advances in Experimental Medicine and Biology, vol 192. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-9442-0_8
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DOI: https://doi.org/10.1007/978-1-4615-9442-0_8
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