Bass A S
Department of Pharmacological and Physiological Sciences, University of Chicago, IL 60637.
Naunyn Schmiedebergs Arch Pharmacol. 1992 Jan;345(1):33-6. doi: 10.1007/BF00175466.
The effects of dopexamine on the vasoconstrictor response to renal nerve stimulation and noradrenaline were determined in anesthetized dogs. Renal vasoconstriction was repeated during the sequential administration of iso-osmotic saline, dopexamine, dopexamine plus the DA1-dopamine receptor antagonist, SCH 23390, and dopexamine plus SCH 23390 and the DA2-dopamine receptor antagonist, domperidone. Renal nerve stimulation-induced vasoconstriction did not change with dopexamine or dopexamine plus SCH 23390, but increased with the addition of domperidone. Dopexamine also potentiated noradrenaline-induced vasoconstriction. Antagonists alone had no affect on the vasoconstrictor response to either stimulus. The findings suggest that the absence of an effect of dopexamine on neuronally-induced renal vasoconstriction was a consequence of a balance between its actions at presynaptic DA2-dopamine receptors (attenuated vasoconstriction) and its ability to inhibit the uptake1 transporter (enhanced vasoconstriction).
在麻醉犬中测定了多培沙明对肾神经刺激和去甲肾上腺素引起的血管收缩反应的影响。在依次给予等渗盐水、多培沙明、多培沙明加DA1 - 多巴胺受体拮抗剂SCH 23390以及多培沙明加SCH 23390和DA2 - 多巴胺受体拮抗剂多潘立酮的过程中,重复进行肾血管收缩实验。肾神经刺激诱导的血管收缩在给予多培沙明或多培沙明加SCH 23390时未发生变化,但在加入多潘立酮后增强。多培沙明还增强了去甲肾上腺素诱导的血管收缩。单独使用拮抗剂对两种刺激引起的血管收缩反应均无影响。这些发现表明,多培沙明对神经源性肾血管收缩无作用是其在突触前DA2 - 多巴胺受体的作用(减弱血管收缩)与其抑制摄取1转运体的能力(增强血管收缩)之间平衡的结果。