Orfila G L, Angel J, Torres M, Barbella Y, Israel A
Faculty of Pharmacy, Department of Biological Sciences, Universidad Central de Venezuela, Caracas.
J Pharm Pharmacol. 1994 May;46(5):397-9. doi: 10.1111/j.2042-7158.1994.tb03825.x.
Intracerebroventricular (i.c.v.) administration of JA116a, induces an increase in urinary volume and sodium excretion in conscious male hydrated rats. The involvement of brain dopaminergic neurons in the JA116a renal action was investigated. Diuretic and natriuretic action of JA116a was blocked by haloperidol pretreatment. The renal effect was prevented by selective dopaminergic neuron, denervation by i.c.v. administration of 6-hydroxydopamine in combination with desmethylimipramine. Our results suggest that JA116a acts centrally, at least in part, via an interaction with endogenous dopamine neurons.
向清醒的雄性水合大鼠脑室内注射JA116a会导致尿量增加和钠排泄增加。研究了脑多巴胺能神经元在JA116a肾脏作用中的参与情况。氟哌啶醇预处理可阻断JA116a的利尿和排钠作用。通过脑室内注射6-羟基多巴胺联合去甲丙咪嗪选择性地使多巴胺能神经元去神经支配，可预防肾脏效应。我们的结果表明，JA116a至少部分地通过与内源性多巴胺神经元相互作用而发挥中枢作用。
