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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Activation of Gi-coupled receptors releases a tonic state of inhibited platelet aggregation.

Single-receptor pharmacology does not satisfactorily explain the physiology of the ADP-induced platelet aggregation response. It has been shown that, in addition to Gq-coupled receptor activation, one Gi-coupled receptor, either the ADP P2T or the alpha2-adrenoceptor, is required for elicitation of aggregation. The underlying mechanism of this action, however, has not been elucidated. By systematically assaying the entire time course of the aggregation and its fade using two methods of aggregometry, we have investigated the role of graded activation of these two Gi-coupled receptors. We demonstrate that constant activation of either of two Gq-coupled receptors, the ADP P2Y1 or the 5-HT2A, and incremental activation of either of the two Gi-coupled receptors, tightly regulates the aggregation response in vitro, through the apparent release of a tonic inhibition of platelet aggregation. This tightly regulated release of inhibition, which appears analogous to the phenomena of disinhibition observed in the central nervous system, may be instrumental for the continuous adaptation of the aggregation response to variable physiological conditions.[1]


  1. Activation of Gi-coupled receptors releases a tonic state of inhibited platelet aggregation. Maayani, S., Schwarz, T., Martinez, R., Tagliente, T.M. Platelets (2001) [Pubmed]
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