Dissociation of the aggregating effect and the inhibitory effect upon cyclic adenosine monophosphate accumulation by adrenaline and adenosine diphosphate in human platelets

Stormorken, Helge; Lyberg, T; Hakvaag, L.; Nakstad, Britt

doi:10.1016/0049-3848(87)90225-8

Cited by 12 publications

(6 citation statements)

References 14 publications

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“…It can be shown both in isolated platelet membranes [220] and in whole cells and is mediated by a GTP-binding protein [220][221][222][223]. The specific G-protein is of G i -subtype; it is directly activated by 2 -adrenoceptor [210][211][212][213] and sensitive to inhibition by pertussis toxin, N -ethylmaleimide and heparin [224][225][226]. Recently, it has been recognized as G i2 by in situ identification with antibodies to Ctermini of the GTP a subunit [220].…”

Section: In Vitro Catecholamine Effectsmentioning

confidence: 99%

“…inhibition of adenylate cyclase activity [203][204][205][206][207][208][209][210][211]; increased turnover of phosphatidylinositol 4,5-bisphosphate (PIP 2 ) and intracellular Ca 2 level through activation of phospholipase C (PLC) [212][213][214][215]; exposure of the fibrinogen receptors [212,[216][217][218][219].…”

mentioning

confidence: 99%

“…1. The inhibition of adenylate cyclase activity is the main consequence of 2 -adrenoceptor stimulation in human platelets [203][204][205][206][207][208][209][210][211]. It can be shown both in isolated platelet membranes [220] and in whole cells and is mediated by a GTP-binding protein [220][221][222][223].…”

mentioning

confidence: 99%

“…The adrenaline effect on adenylate cyclase-responsible for decrease of intraplatelet basal cAMP content and interference with the responses to PGE 1 , forskolin and prostacylin [143,179,206]-could allow platelets to be more easily activated; however, different reports indicate that it is probably not essential for platelet activation [108,133,210,211,213,230,231].…”

mentioning

confidence: 99%

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Role of catecholamines in platelet function: pathophysiological and clinical significance

Anfossi

Trovati

1996

Eur J Clin Investigation

166

107

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Platelets are involved in the pathogenesis of vascular damage in both atherosclerosis and arterial hypertension. Their reactivity in vivo is influenced by different factors, including sympathoadrenal activation, plasma levels of atherogenic lipoproteins and haemorrheological changes. In the present review, we examine the modulation of platelet function by the sympathoadrenal system and concentrate on the role of circulating catecholamines in the control of platelet responses. Human platelets exhibit both adrenergic and dopaminergic receptors that are influenced by different catecholamines. alpha(2)-Adrenoceptors of alpha(2A) subtype prevail on platelet membrane; through their stimulation, catecholamines potentiate the effects of other agonists and, at higher concentrations, initiate platelet responses, including aggregation, secretion and arachidonate pathway activation. Physiological and pathological conditions causing sympathoadrenal activation in vivo, i.e. physical activity, mental stress, insulin-induced hypoglycaemia, acute coronary ischaemia and heart failure, modify the circulating platelet populations and modulate platelet reactivity through an increase in circulating catecholamines. A sympathoadrenal hyperactivation modifies the function of circulating platelets through direct catecholamine effects, catecholamine-induced changes of haemodynamic factors and lipid pattern and inhibition of the vascular eicosanoid synthesis. The catecholamine effects on platelet function can be involved in the interplay among stress, adrenomedullary system activation and cardiovascular diseases.

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Section: In Vitro Catecholamine Effectsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Role of catecholamines in platelet function: pathophysiological and clinical significance

Anfossi

Trovati

1996

Eur J Clin Investigation

166

107

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“…On the other hand, other investigators reported normal numbers of a2-adrenergic receptors in a large number of such MPD patients [24]. Re- garding the coupling of a,-adrenergic receptors to adenylate cyclase, many investigators reported that there was no abnormality in epinephrine-insensitive platelets from MPD patients [18] and other subjects [23,25,26]. Our data on the epinephrine-induced inhibition of PGE,-induced cAMP elevation in the platelets from both epinephrine-sensitive and -insensitive MPD patients as well as from normal subjects were in support of these reports.…”

Section: Discussionmentioning

confidence: 96%

Deficient elevation of the cytoplasmic calcium ion concentration by epinephrine in epinephrine‐insensitive platelets of patients with myeloproliferative disorders

Ushikubi¹,

Okuma²,

Ishibashi³

et al. 1990

American J Hematol

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Elevation of the cytoplasmic Ca2+ concentration ([Ca2+]i) by epinephrine and epinephrine-induced inhibition of prostaglandin E1 (PGE1)-stimulated cyclic adenosine monophosphate (cAMP) accumulation were assessed in platelets from three groups of subjects; normal controls (NS, n = 11) and patients with myeloproliferative disorders whose platelets were either sensitive (ES, n = 9) or specifically insensitive (El, n = 7) to the aggregatory effect of epinephrine. The inhibition by epinephrine of cAMP accumulation in the platelets exposed to 500 nM PGE1 was not significantly different between the three groups. Therefore, despite the defective aggregation response to epinephrine, platelets from the El group seemed to retain normal response, which was attained through alpha 2-adrenergic receptors, guanine nucleotide binding regulatory protein, and the adenylate cyclase system. However, in aequorin-loaded, washed platelets, the epinephrine-stimulated rise in [Ca2+]i showed significant decrease in the El group compared with the other groups (P less than 0.01). Thus the mechanism for the impaired aggregation response to epinephrine in platelets from the El group could include the defect that exists in the pathway from receptor binding of epinephrine to the aggregation response through [Ca2+]i elevation.

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Inhibition of platelet aggregation by prostacyclin is attenuated after exercise in patients with angina pectoris

Kishi

Ashikaga

Numano

1992

American Heart Journal

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Dissociation of the aggregating effect and the inhibitory effect upon cyclic adenosine monophosphate accumulation by adrenaline and adenosine diphosphate in human platelets

Cited by 12 publications

References 14 publications

Role of catecholamines in platelet function: pathophysiological and clinical significance

Role of catecholamines in platelet function: pathophysiological and clinical significance

Deficient elevation of the cytoplasmic calcium ion concentration by epinephrine in epinephrine‐insensitive platelets of patients with myeloproliferative disorders

Inhibition of platelet aggregation by prostacyclin is attenuated after exercise in patients with angina pectoris

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