In vitro effects of the selective dopamine 1-agonist fenoldopam on the coagulation system in native whole blood: Comparison to dopamine and nitroprusside

Lorenz, Reinhard; Paschke, Carola; Born, Peter; Clemens, Ralf

doi:10.1016/0049-3848(95)90871-c

Cited by 2 publications

(2 citation statements)

References 14 publications

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“…It has been used clinically in the treatment of congestive heart failure, myocardial dysfunction, shock and Parkinson's disease (Goldberg, 1972; Tarazi, 1974). At high doses, dopamine causes vasoconstriction and impaired renal function (Lorenz et al , 1995). Specific dopamine receptor agonists have been shown to elicit the beneficial effects of vasodilatation, lowered blood pressure and increased kidney perfusion (Frederickson et al , 1985; Hughes et al , 1986; Elliott et al , 1990) without the side‐effects associated with dopamine (Shusterman, 1993).…”

Section: Introductionmentioning

confidence: 99%

Effects of dopamine and selective dopamine agonists upon platelet accumulation in the cerebral and pulmonary vasculature of the rabbit

Emerson

Paul

Ferlenga

et al. 1997

British J Pharmacology

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1 A selection of novel compounds were shown to exhibit dopaminergic activity in vitro. 2 111 Indium-labelled platelets were continuously monitored in the cerebral and pulmonary vasculature of anaesthetized rabbits. The e ects of dopamine and selective dopamine receptor agonists on ADP and thrombin induced platelet accumulation were recorded. 3 Pretreatment with dopamine (2 mg kg 71 min 71 , i.v.) signi®cantly reduced ADP (20 mg kg 71 , i.v.) induced platelet accumulation in the pulmonary vasculature whereas lower doses had no e ect. 4 Dopamine (100 mg kg 71 min 71 intra-carotid, i.c.) potentiated thrombin (90 u kg 71 , i.c.) induced platelet accumulation in the cerebral vasculature whereas higher doses (1 ± 2 mg kg 71 min 71 ) inhibited accumulation. 5 The selective dopamine receptor agonists tested did not signi®cantly inhibit platelet accumulation induced by ADP or thrombin. Two of these selective agonists, at doses higher than the intended therapeutic doses, induced thrombocytopaenia and an associated increase in platelet accumulation in the lung in response to thrombin. 6 These results extend previous in vitro studies regarding the dual actions of dopamine upon platelets and show for the ®rst time the e ects of selective dopamine receptor agonists upon platelet aggregation in vivo.

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Section: Introductionmentioning

confidence: 99%

Effects of dopamine and selective dopamine agonists upon platelet accumulation in the cerebral and pulmonary vasculature of the rabbit

Emerson

Paul

Ferlenga

et al. 1997

British J Pharmacology

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show abstract

“…Dopamine has been used clinically in the treatment of congestive heart failure, myocardial dysfunction, shock and Parkinson's disease ( Goldberg, 1972 ; Tarazi, 1974 ), but at high doses causes side‐effects such as increased blood pressure and impaired renal function ( Lorenz et al ., 1995 ). Specific dopamine agonists have been shown to elicit the beneficial effects of dopamine ( Frederickson et al ., 1985 ; Hughes et al ., 1986 ; Elliott et al ., 1990 ) without the associated side‐effects ( Shusterman et al ., 1993 ).…”

Section: Introductionmentioning

confidence: 99%

Regulation of platelet function by catecholamines in the cerebral vasculature of the rabbit

Emerson

Paul

Page

1999

British J Pharmacology

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In-labelled platelets were monitored continuously in the cerebral and pulmonary vascular beds of anaesthetized rabbits. Dopamine can, depending upon the concentration, either potentiate or inhibit thrombin-induced platelet accumulation in the cerebral vasculature of rabbits by unknown mechanisms. The eects of speci®c adrenergic and dopaminergic receptor antagonists were tested upon dopamine's actions on intracarotid (i.c.) thrombin-induced (80 u kg 71 ) platelet accumulation in the cerebral vasculature. The eect of adrenaline on the response to thrombin in this vascular bed was also investigated. 2 Thrombin-induced platelet accumulation was signi®cantly (P50.01) potentiated by dopamine (100 mg kg 71 min 71 , i.c.) and this eect was signi®cantly inhibited by infusion of the a-adrenoceptor antagonist, phentolamine. 3 A higher dose of dopamine (2 mg kg 71 min 71, i.c.) inhibited thrombin-induced platelet accumulation. The b-adrenoceptor antagonist, propranolol, did not signi®cantly alter this inhibitory eect whereas it was abolished by the dopamine D1 selective antagonist, SCH23390. 4 Adrenaline (when administered i.c. by bolus injection or infusion) had no signi®cant eect on thrombin-induced accumulation at any of the doses tested. 5 Potentiation of in vivo platelet accumulation by dopamine therefore seems to occur via aadrenergic receptors. However, the inhibitory eect of dopamine appears to be exerted via the activation of dopamine D1 receptors and not via b-adrenergic receptors. Our ®ndings con®rm that dopamine, but not adrenaline, can modify platelet function in the cerebral vasculature and these observations may have implications for current and potential therapeutic uses of dopamine and selective dopaminergic compounds.

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In vitro effects of the selective dopamine 1-agonist fenoldopam on the coagulation system in native whole blood: Comparison to dopamine and nitroprusside

Cited by 2 publications

References 14 publications

Effects of dopamine and selective dopamine agonists upon platelet accumulation in the cerebral and pulmonary vasculature of the rabbit

Effects of dopamine and selective dopamine agonists upon platelet accumulation in the cerebral and pulmonary vasculature of the rabbit

Regulation of platelet function by catecholamines in the cerebral vasculature of the rabbit

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