Mehrabani P A, Bassett J R
School of Biological Sciences, Macquarie University, N.S.W., Australia.
Pharmacol Biochem Behav. 1988 Jun;30(2):391-6. doi: 10.1016/0091-3057(88)90473-x.
Spontaneously beating rat atria were incubated with 3H-norepinephrine both in the presence and absence of (1-24)ACTH. A significant reduction in the uptake and retention of radioactivity was found in atria pretreated with (1-24)ACTH. A kinetic study of the uptake process showed similar Km values for both the control (24.1 x 10(-8) M) and (1-24)ACTH pretreated (22.2 x 10(-8) M) groups, but a significantly different Vmax. The Km values were similar to that reported for the neuronal reuptake process (Uptake 1). It was concluded that the ACTH-induced enhanced myocardial sensitivity to catecholamines previously reported, could be explained in part on the basis of an inhibition of neuronal uptake by (1-24)ACTH. The inhibition of neuronal uptake by (1-24)ACTH was dose-dependent.
将自发性搏动的大鼠心房分别在存在和不存在(1-24)促肾上腺皮质激素(ACTH)的情况下与3H-去甲肾上腺素一起孵育。在用(1-24)ACTH预处理的心房中发现放射性摄取和保留显著减少。摄取过程的动力学研究表明,对照组(24.1×10⁻⁸ M)和(1-24)ACTH预处理组(22.2×10⁻⁸ M)的Km值相似,但Vmax显著不同。这些Km值与报道的神经元再摄取过程(摄取1)的值相似。得出的结论是,先前报道的ACTH诱导的心肌对儿茶酚胺敏感性增强,部分可以基于(1-24)ACTH对神经元摄取的抑制来解释。(1-24)ACTH对神经元摄取的抑制是剂量依赖性的。