Platelet ADP/Purinergic Receptors

Gachet, Christian; Cazenave, J.-P.

doi:10.1007/978-3-642-60639-7_6

Platelets and Their Factors

1997

DOI: 10.1007/978-3-642-60639-7_6

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Platelet ADP/Purinergic Receptors

Christian Gachet¹,

J.-P. Cazenave²

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Cited by 2 publications

References 86 publications

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Activation of G i -coupled receptors releases a tonic state of inhibited platelet aggregation

et al. 2001

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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.

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Activation of G i -coupled receptors releases a tonic state of inhibited platelet aggregation

et al. 2001

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Marked Temperature Dependence of the Platelet Calcium Signal Induced by Human von Willebrand Factor

Kermode

Zheng

Milner

1999

Blood

112

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Interaction of von Willebrand factor (vWF) with the platelet is essential to hemostasis when vascular injury occurs. This interaction elevates the intracellular free calcium concentration ([Ca2+]i) and promotes platelet activation. The present study investigated the temperature dependence of vWF-induced [Ca2+]i signaling in human platelets. The influence of temperature can provide invaluable insight into the underlying mechanism. Platelet [Ca2+]i was monitored with Fura-PE3. Ristocetin-mediated binding of vWF induced a transient platelet [Ca2+]i increase at 37°C, but no response at lower temperatures (20°C to 25°C). This temperature dependence could not be attributed to a reduction in vWF binding, as ristocetin-mediated platelet aggregation and agglutination were essentially unaffected by temperature. Most other platelet agonists (U-46619, -thrombin, and adenosine 5′-diphosphate [ADP]) induced a [Ca2+]isignal whose amplitude did not diminish at lower temperatures. The [Ca2+]i signal in response to arachidonic acid, however, showed similar temperature dependence to that seen with vWF. Assessment of thromboxane A2 production showed a strong temperature dependence for metabolism of arachidonic acid by the cyclo-oxygenase pathway. vWF induced thromboxane A2production in the platelet. Aspirin treatment abolished the vWF-induced [Ca2+]i signal. These observations suggest that release of arachidonic acid and its conversion to thromboxane A2 play a central role in vWF-mediated [Ca2+]i signaling in the platelet at physiological temperatures.

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Platelet ADP/Purinergic Receptors

Cited by 2 publications

References 86 publications

Activation of G i -coupled receptors releases a tonic state of inhibited platelet aggregation

Activation of G i -coupled receptors releases a tonic state of inhibited platelet aggregation

Marked Temperature Dependence of the Platelet Calcium Signal Induced by Human von Willebrand Factor

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