血管紧张素改变牛肾上腺球状带细胞中的45Ca2+通量。
Angiotensin alters 45Ca2+ fluxes in bovine adrenal glomerulosa cells.
作者信息
Elliott M E, Goodfriend T L
出版信息
Proc Natl Acad Sci U S A. 1981 May;78(5):3044-8. doi: 10.1073/pnas.78.5.3044.
Abstract
Angiotensin II stimulated 45Ca2+ release from bovine adrenal glomerulosa cells. It also decreased the influx of 45Ca2+ into glomerulosa cells. The effects were observed within 2 min of hormone addition and were blocked by Saralasin a competitive inhibitor of angiotensin. Des-Phe8-angiotensin II, a biologically inert analog, was inactive in this system. Angiotensin II also inhibited the influx of 133Ba2+ and 54Mn2+, whereas 51Cr6+ and 57Co2+ were unaffected. Alterations in 45Ca2+ fluxes were seen with concentrations of angiotensin that stimulate aldosterone biosynthesis in bovine glomerulosa cell preparations. These results suggest that calcium plays a key role in angiotensin-stimulated aldosteronogenesis.
摘要
血管紧张素II刺激牛肾上腺球状带细胞释放45Ca2+。它还减少了45Ca2+流入球状带细胞。在添加激素后2分钟内观察到这些效应，并且被血管紧张素的竞争性抑制剂沙拉新所阻断。去苯丙氨酸8-血管紧张素II是一种无生物活性的类似物，在该系统中无活性。血管紧张素II还抑制133Ba2+和54Mn2+的流入，而51Cr6+和57Co2+不受影响。在能刺激牛球状带细胞制剂中醛固酮生物合成的血管紧张素浓度下，观察到45Ca2+通量的变化。这些结果表明钙在血管紧张素刺激的醛固酮生成中起关键作用。
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