1993
DOI: 10.1055/s-0038-1649614
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The Platelet-Stimulating Effect of Adrenaline Through α2-Adrenergic Receptors Requires Simultaneous Activation by a True Stimulatory Platelet Agonist

Abstract: SummaryThe stimulating effect of adrenaline on human platelet phospholipase C (PLC) activation and responses in vitro (shape change, aggregation and dense granule secretion) was investigated with respect to its dependence on exogenously added agonists. All experiments were performed with human gel-filtered platelets pretreated with acetylsalicylic acid to prevent endogenous stimulation by the arachidonate pathway. (1) Preliminary experiments demonstrated the presence of trace amounts of extracellular ADP (0.05… Show more

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Cited by 70 publications
(57 citation statements)
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“…15 It has been reported that epinephrine serves primarily to increase platelet aggregation induced by other autocoids. 16 Our data on the effect of epinephrine on potentiating thrombininduced platelet aggregation were striking. It remains to be determined whether epinephrine acts synergistically with other autocoids in addition to thrombin in facilitating thrombosis.…”
Section: Discussionmentioning
confidence: 83%
“…15 It has been reported that epinephrine serves primarily to increase platelet aggregation induced by other autocoids. 16 Our data on the effect of epinephrine on potentiating thrombininduced platelet aggregation were striking. It remains to be determined whether epinephrine acts synergistically with other autocoids in addition to thrombin in facilitating thrombosis.…”
Section: Discussionmentioning
confidence: 83%
“…On the other hand, analogous to the P2T AC receptor activation, epinephrine causes inhibition of adenylyl cyclase, through activation of the ␣ 2A -adrenergic receptors on platelets. Epinephrine, which promotes only inhibition of adenylyl cyclase, by coupling to G i , does not cause platelet aggregation, although it potentiates platelet aggregation induced by other agonists, which activate G q (35,36). As shown in Fig.…”
Section: Cell Biology: Jin and Kunapulimentioning
confidence: 85%
“…Although the P2Y1 receptor alone can mediate ADPinduced platelet shape change (9), signaling events from both the P2Y1 and P2T AC receptors are essential for ADP-induced platelet aggregation. This model also explains the inability of epinephrine to cause platelet aggregation in the absence of positive feedback from thromboxane A 2 or ADP, although it can potentiate other platelet-aggregating agents (35,36). We propose that concomitant signaling through G i and G q is the general mechanism by which fibrinogen receptor activation and subsequent platelet aggregation occurs.…”
mentioning
confidence: 75%
“…The simultaneous addition of subthreshold concentrations of 5-HT (1-2 μM) and epinephrine (0.5-1 μM) exhibited synergistic e ffect ( Figure 2A). 5-HT is considered a weak platelet agonist as it causes only shape change in platelets (Steen et al, 1993), however, subthreshold concentrations of 5-HT and epinephrine, when used together, can elicit a strong synergistic effect on platelet aggregation. Such a mechanism of synergism is known among other agonists too and is considered to occur due to activation of Ca 2+ signalling cascade.…”
Section: Resultsmentioning
confidence: 99%
“…Receptors for 5-HT in platelets are coupled with Gq/ PLC (De Chaffoy de Courcelles et al, 1987;Martin, 1994) whereas epinephrine interacts with α 2 -a d r e n o c e p t o r s coupled with Gi/adenylyl cyclase pathway (Steen et al ., 1993). Recent studies show that β γ-subunits of activated Gi protein can also activate PLC (Clapham and Neer, 1997;Banno et al, 1998).…”
Section: Resultsmentioning
confidence: 99%