pubmed:abstractText |
This study was undertaken to investigate the mechanism of the tachycardic effect of bromocriptine, a specific dopamine D-2 receptor agonist, which is not abolished, as previously reported, by intravenous domperidone, a selective dopamine D-2 antagonist unable to cross the blood brain barrier. Two hypotheses were tested: (1) that the increase in heart rate after intravenous treatment with bromocriptine could be related to central dopamine receptor stimulation and (2) that it could be induced by a release of adrenaline from the adrenal medulla.
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