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• W2079223047 abstract "The effects of dopamine, (±)-dobutamine (racemic mixture) and (–)-dobutamine on α-adrenoceptor-mediated vasoconstriction were evaluated in the pulmonary circulation of the anesthetized dog. The drugs were studied in the absence and presence of pro-pranolol (1 mg/kg, i.v.) in order to assess β-adrenoceptor-mediated effects in the pulmonary circulation. Intra-arterial administration of dopamine, (±)-dobutamine and (–)-dobutamine elicited dose-dependent increases in pulmonary perfusion pressure, reflecting increases in pulmonary vascular resistance. In control animals, dopamine elicited the largest increases in pulmonary perfusion pressure (45% above resting pulmonary pressure) followed by (–)-dobutamine (30% increase) and (±)-dobutamine (15% increase). The pressor effects of dopamine in the pulmonary circulation were mediated by both postjunctional vascular α₁<i>-</i>and α₂-adrenoceptors, since prazosin, (100 μg/kg, i.v.), a selective α₁-adrenoceptor antagonist, and rauwolscine (100 μg/kg, i.v.), a selective α₁-adrenoceptor antagonist, both inhibited the vasopressor response elicited by dopamine to roughly equivalent degrees. Pulmonary vasoconstriction produced by (±)-dobutamine and (–)-dobutamine was mediated primarily by postsynaptic vascular α₁-adrenoceptors, although α₂-adrenoceptor-mediated vasoconstriction was observed. In propranolol-pretreated animals, the increase in pulmonary perfusion pressure elicited by dopamine and (–)-dobutamine was qualitatively and quantitatively similar to that observed in control animals, suggesting that these agents have little activity on vascular β₂-adrenoceptors in the pulmonary circulation. In marked contrast, the maximum pulmonary vasopressor response obtained with (±)-dobutamine were greater in propranolol-pretreated animals, indicating that (±)-dobutamine also has the capacity to stimulate pulmonary vascular β₂-adrenoceptors which mediate pulmonary vasodilation that, in part, mask α-adrenoceptor-mediated pulmonary vasoconstriction. Since the (–)-enantiomer of dobutamine has little or no β₂-adrenoceptor agonist activity, the β₂-adrenoceptor-mediated effect of (±)-dobutamine must result from the (+)-enantiomer as has been previously proposed. The results of the present study indicate that dopamine has a greater propensity for increasing pulmonary vascular resistance, and therefore pulmonary arterial blood pressure, relative to (±)-dobutamine. This results, at least in part, from the relatively weaker activity of dopamine in stimulating pulmonary vascular β₂-adrenoceptors which mediate vasodilation. This, in turn, shifts the balance of activity for dopamine in favor of activating pulmonary vascular α₁ and α₂-adrenoceptors to produce vasoconstriction. The results are consistent with, and may even account for, the clinical observation that dopamine is far more likely to increase pulmonary capillary wedge pressure and pulmonary vascular resistance in patients with congestive heart failure than is (±)-dobutamine, and that the β₂-adrenoceptor agonist activity of (±)-dobutamine may be critical for the beneficial effects of this drug in the pulmonary circulation." @default.
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• W2079223047 title "Interaction of Dopamine, (±)-Dobutamine and the (–)-Enantiomer of Dobutamine with α- and β-Adrenoceptors in the Pulmonary Circulation of the Dog" @default.
• W2079223047 doi "https://doi.org/10.1159/000138270" @default.
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