Apfeldorf W J, Isales C M, Barrett P Q
Department of Cell Biology, Yale University School of Medicine, New Haven, Connecticut 06510.
Endocrinology. 1988 Apr;122(4):1460-5. doi: 10.1210/endo-122-4-1460.
The effect of atrial natriuretic peptide (ANP) on cellular calcium metabolism was evaluated in bovine adrenal glomerulosa cells stimulated by agonists that use the Ca2+-phosphoinositide messenger system. The calcium-sensitive probe aequorin was used to measure intracellular free calcium concentration, and the aldosterone secretory rate was simultaneously monitored. ANP did not block the calcium transient induced by beta-[Asp1]angiotensin II (beta-[Asp1]AII), an AII analog, but markedly reduced the stimulated rate of aldosterone secretion. Consistent with these findings, radiolabeled 45Ca efflux stimulated by AII and carbachol was not altered by the concurrent addition of ANP. These results indicate that ANP has no effect on the phosphoinositide-mediated calcium transient and the associated rise in cellular calcium efflux, suggesting that these parameters of calcium metabolism are not the locus of ANP's inhibitory action.
在使用Ca2+-磷酸肌醇信使系统的激动剂刺激的牛肾上腺球状带细胞中，评估了心房利钠肽（ANP）对细胞钙代谢的影响。使用钙敏感探针水母发光蛋白测量细胞内游离钙浓度，并同时监测醛固酮分泌率。ANP不会阻断AII类似物β-[天冬氨酸1]血管紧张素II（β-[天冬氨酸1]AII）诱导的钙瞬变，但会显著降低刺激后的醛固酮分泌率。与这些发现一致，AII和卡巴胆碱刺激的放射性标记45Ca外流在同时添加ANP时未发生改变。这些结果表明，ANP对磷酸肌醇介导的钙瞬变和细胞钙外流的相关增加没有影响，这表明钙代谢的这些参数不是ANP抑制作用的位点。
