Morphine and Apomorphine Inhibit Gastrointestinal Transit [GIT] Through Two Different Mechanisms

Morphine was used as a remedy for the control of diarrhea centuries before it's sedative-analgesic effect was discovered. Although several mechanisms have been proposed for the morphine-induced inhibition of gastrointestinal transit [GIT], the exact mechanism has not yet been identified. On this basis the possible involvement of the dopaminergic system in morphine-induced inhibition of transit was investigated. This study showed that morphine decreased gastrointestinal transit [GIT] of charcoal dust in mice in a dose-dependent manner. The response was inhibited by the opiate antagonist naloxone. Pretreatment of animals with the D-2 antagonist sulpiride or the peripheral dopamine antagonist domperidone did not alter the morphine-induced inhibition of GIT. The D-l/D-2 agonist apomorphine also decreased GIT in mice. The response was inhibited by SCH 23390 or sulpiride pretreatment [p<0.01], but not by domperidone or naloxone. It is concluded that morphine and apomorphine inhibit GIT through opiate and dopaminergic mechanisms, respectively

Reversal by indomethacin of renal effects of dopamine in subjects with normal renal function

En 5 sujetos con función renal normal, la administración intravenosa de dopamina a una tasa de 6 ug/kg/m, produjo vasodilatación renal, incrementó la excreción urinaria de Na y redujo la osmolaridad urinaria, sin modificar la filtración glomerular. Estos efectos fueron revertidos con la administración intravenosa de indometacina (2 mg/kg), sugiriendo que los efectos renales de la dopamina podrían depender de una producción normal de prostaglandinas