Lynch C J, Deth R C
Pharmacology. 1984;28(2):74-85. doi: 10.1159/000137952.
The effects of alpha-adrenergic agonists on 45Ca efflux from slices of rat liver were studied and the results compared to earlier studies on the rabbit aorta. Norepinephrine and phenylephrine (PE) cause a stimulation of 45Ca efflux which was due to alpha 1-receptor activation. The mitochondrial uncoupler dinitrophenol (DNP) also stimulated 45Ca efflux while caffeine had little or no effect. PE and DNP effects were due to the release of intracellular 45Ca stores, and both agents released a similar quantity of Ca2+. 45Ca/40Ca exchange in both PE- and DNP-released sources was similar (t1/2 approximately or equal to 16 min). DNP and PE effects were not additive, and previous exposure to one agent reduces the response to the other. These results suggest that alpha 1-agonists and DNP release a common source of intracellular Ca2+ in rat liver. Since in rabbit aorta alpha-agonists primarily release Ca2+ from a nonmitochondrial source, our results suggest alpha 1-receptors act via the generation of a Ca2+-releasing substance which subsequently mobilizes Ca2+ from different organelles in different tissues.
研究了α-肾上腺素能激动剂对大鼠肝脏切片中45Ca流出的影响，并将结果与早期对兔主动脉的研究进行了比较。去甲肾上腺素和去氧肾上腺素（PE）可刺激45Ca流出，这是由于α1受体激活所致。线粒体解偶联剂二硝基苯酚（DNP）也能刺激45Ca流出，而咖啡因的影响很小或没有影响。PE和DNP的作用是由于细胞内45Ca储存的释放，两种药物释放的Ca2+量相似。PE和DNP释放源中的45Ca/40Ca交换相似（半衰期约为16分钟）。DNP和PE的作用不是相加的，先前接触一种药物会降低对另一种药物的反应。这些结果表明，α1激动剂和DNP在大鼠肝脏中释放共同的细胞内Ca2+源。由于在兔主动脉中，α激动剂主要从非线粒体源释放Ca2+，我们的结果表明α1受体通过产生一种Ca2+释放物质起作用，该物质随后从不同组织的不同细胞器中动员Ca2+。
