Angiotensin alters 45Ca2+ fluxes in bovine adrenal glomerulosa cells.
Angiotensin alters 45Ca2+ fluxes in bovine adrenal glomerulosa cells.
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血管紧张素改变牛肾上腺肾小球细胞中的 45Ca2 通量。
DOI：
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发表时间：
1981
影响因子：
11.1
通讯作者：
William S. Middleton
中科院分区：
文献类型：
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作者：
M. Elliott;T. Goodfriend;William S. Middleton
血管紧张素II刺激牛肾上腺肾小球细胞45 Ca ~（2+）释放。减少~（45）Ca ~（2+）内流。在激素添加后2分钟内观察到这种作用，并被血管紧张素竞争性抑制剂Saralasin阻断。Des-Phe 8-血管紧张素II，一种生物惰性类似物，在该系统中无活性。血管紧张素Ⅱ也抑制~（133）Ba ~（2+）和~（54）Mn ~（2+）的内流，而~（51）Cr ~（6+）和~（57）Co ~（2+）则不受影响。在牛肾小球细胞制剂中，45 Ca 2+通量的改变与刺激醛固酮生物合成的血管紧张素浓度有关。这些结果表明，钙在血管紧张素刺激的醛固酮生成中起着关键作用。
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.