Lam B K, Stier C T, Wynn N C, Itskovitz H D
J Cardiovasc Pharmacol. 1986 May-Jun;8(3):554-8. doi: 10.1097/00005344-198605000-00018.
The ability of l-dopa and dopamine to modulate renal vascular responses to norepinephrine (NE, 50-150 ng) was examined in isolated Tyrode-perfused kidneys from male Sprague-Dawley rats. Renal pressor responses to bolus injections of NE were constant during saline infusion. In contrast, l-dopa (15 micrograms/min and 75 micrograms/min) and dopamine (15 micrograms/min) infusions that did not alter baseline perfusion pressure increased pressor responses to NE significantly. Concomitant infusion of the aromatic l-amino-acid decarboxylase inhibitor carbidopa (20 micrograms/min) suppressed the ability of l-dopa (75 micrograms/min) but not dopamine to enhance renal pressor responses to NE. The pressor potentiation of NE did not appear to be the result of a general musculotropic effect or altered alpha-1 adrenoreceptor activity since increased vasoconstrictor responses to phenylephrine (PE) and serotonin (5-HT) were not observed. Infusions of cocaine (15 micrograms/min) enhanced the renal pressor effects of NE but not PE in similar fashion to l-dopa and dopamine. In the presence of cocaine, l-dopa did not potentiate NE constriction further. These results suggest that endogenous or exogenous dopamine in the kidney may affect neuronal NE uptake to enhance its renal vascular effects.
在来自雄性斯普拉格 - 道利大鼠的离体台氏液灌注肾脏中,研究了左旋多巴和多巴胺调节肾脏血管对去甲肾上腺素(NE,50 - 150纳克)反应的能力。在输注生理盐水期间,对推注NE的肾脏升压反应是恒定的。相比之下,输注不改变基线灌注压力的左旋多巴(15微克/分钟和75微克/分钟)和多巴胺(15微克/分钟)会显著增加对NE的升压反应。同时输注芳香族左旋氨基酸脱羧酶抑制剂卡比多巴(20微克/分钟)可抑制左旋多巴(75微克/分钟)增强肾脏对NE升压反应的能力,但不影响多巴胺。NE的升压增强作用似乎不是一般的促肌性效应或α-1肾上腺素能受体活性改变的结果,因为未观察到对去氧肾上腺素(PE)和5-羟色胺(5-HT)的血管收缩反应增加。输注可卡因(15微克/分钟)以类似于左旋多巴和多巴胺的方式增强了NE的肾脏升压作用,但不增强PE的作用。在存在可卡因的情况下,左旋多巴不会进一步增强NE的收缩作用。这些结果表明,肾脏中的内源性或外源性多巴胺可能会影响神经元对NE的摄取,以增强其对肾脏血管的作用。