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多巴胺和左旋多巴对去甲肾上腺素在离体灌注大鼠肾脏中升压反应的增强作用。

Dopamine and L-dopa potentiation of pressor responses to norepinephrine in isolated perfused rat kidneys.

作者信息

Lam B K, Stier C T, Wynn N C, Itskovitz H D

出版信息

J Cardiovasc Pharmacol. 1986 May-Jun;8(3):554-8. doi: 10.1097/00005344-198605000-00018.

Abstract

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.

摘要

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。

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