Eisenhofer G, McCarty R, Pacak K, Russ H, Schömig E
Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institute of Health, Bethesda, MD 20892-1424, USA.
Naunyn Schmiedebergs Arch Pharmacol. 1996 Aug-Sep;354(3):287-94. doi: 10.1007/BF00171059.
The role of extraneuronal uptake in terminating the actions of catecholamines has been difficult to evaluate in vivo, largely because of lack of suitable inhibitors. The compound, 1,1'-diisopropyl-2,4'-cyanine iodide or disprocynium24 (D24), is a novel inhibitor of extraneuronal uptake with a high degree of potency in vitro. This study examined the actions of D24 on the inactivation and metabolism of circulating noradrenaline and adrenaline in conscious rats. Animals received i.v. infusions of 3H-labelled noradrenaline and adrenaline, and their extraneuronal O-methylated metabolites, normetanephrine and metanephrine. Plasma concentrations of endogeneous and 3H-labelled catecholamines and metanephrines were measured before and after D24. D24 caused large increases in plasma concentrations of noradrenaline and adrenaline, effects due to both decreases in their plasma clearances and increases in their rates of release into plasma. Plasma concentrations of normetanephrine and metanephrine also increased due to their decreased clearance from plasma. Increased release of normetanephrine into plasma did not contribute to increased plasma concentrations of normetanephrine. In fact, the contribution of extraneuronal O-methylation to noradrenaline clearance decreased substantially after D24. The data indicate that D24 is a potent inhibitor of the extraneuronal catecholamine transporter in vivo and that this process contributes importantly to the removal of circulating catecholamines and their O-methylated amine metabolites. Increased release of noradrenaline into plasma may reflect an increase in the proportion of transmitter that escapes from sites of release into the circulation. However, increased adrenaline release indicates that the drug also causes sympathoadrenal activation.
由于缺乏合适的抑制剂,在体内评估非神经元摄取在终止儿茶酚胺作用中的角色一直很困难。化合物1,1'-二异丙基-2,4'-氰化碘或双丙氰铵24(D24)是一种新型的非神经元摄取抑制剂,在体外具有高度的效力。本研究检测了D24对清醒大鼠体内循环去甲肾上腺素和肾上腺素的失活及代谢的作用。动物静脉注射3H标记的去甲肾上腺素和肾上腺素及其非神经元O-甲基化代谢产物去甲变肾上腺素和变肾上腺素。在给予D24前后测量内源性和3H标记的儿茶酚胺及变肾上腺素的血浆浓度。D24导致去甲肾上腺素和肾上腺素的血浆浓度大幅升高,这是由于它们的血浆清除率降低以及释放到血浆中的速率增加所致。去甲变肾上腺素和变肾上腺素的血浆浓度也因它们从血浆中的清除率降低而升高。去甲变肾上腺素释放到血浆中的增加对其血浆浓度升高没有贡献。事实上,在D24作用后,非神经元O-甲基化对去甲肾上腺素清除的贡献大幅降低。数据表明,D24在体内是一种有效的非神经元儿茶酚胺转运体抑制剂,并且该过程对循环儿茶酚胺及其O-甲基化胺代谢产物的清除起着重要作用。去甲肾上腺素释放到血浆中的增加可能反映了从释放部位逃逸到循环中的递质比例增加。然而,肾上腺素释放增加表明该药物还会引起交感肾上腺激活。