RESUMEN
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
Asunto(s)
Animales de Laboratorio , Apomorfina/farmacología , Tránsito Gastrointestinal/efectos de los fármacos , Ratones , Dopamina , Dopamina/antagonistas & inhibidores , DopaminaRESUMEN
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