Endothelin evoked Ca2+ transients and oscillations in A10 vascular smooth muscle cells.
Endothelin evoked Ca2+ transients and oscillations in A10 vascular smooth muscle cells.
复制标题
内皮素在 A10 血管平滑肌细胞中引起 Ca2 瞬变和振荡。
DOI：
10.1016/0006-291x(89)91108-x
复制
发表时间：
1989
影响因子：
3.1
通讯作者：
C. Ashley
中科院分区：
文献类型：
--
作者：
A. W. Simpson;C. Ashley
内皮素（200 nM）引起[Ca 2 +] i迅速升高，随后[Ca 2 +]i持续升高。最初的瞬变可以通过释放储存的Ca 2+来解释，而维持的平台期可能是Ca 2+的内流，因为它被硝苯地平（5 μM）部分抑制，剩余的成分被细胞外Ca 2+的清除所消除。加压素（1 nM）诱发了类似的反应，也显示了硝苯地平不敏感的成分，它的平台期。内皮素也诱发振荡[Ca 2 +]i;这些特征在于由一个快速上升阶段，然后缓慢下降，没有“起搏器”上升[Ca 2 +] prereceding上升阶段。通过加入5μM硝苯地平或去除细胞外Ca 2+抑制振荡，表明它们至少部分依赖于电压门控Ca 2+内流。
Endothelin (200 nM) evoked a rapid rise in [Ca2+]iwhich was then followed by a maintained elevation of [Ca2+]i. The initial transient can be explained by the release of stored Ca2+whilst the maintained plateau is likely to be an influx of Ca2+as it was partially inhibited by nifedipine (5 μM) and the remaining component abolished by the removal of extracellular Ca2+. Vasopressin (1 nM) evoked a similar response which also showed a nifedipine insensitive component to it's plateau phase. Endothelin also evoked oscillations in [Ca2+]i; these where characterised by a rapid rising phase followed by a slower decline, with no ‘pacemaker’ rise in [Ca2+]ipreceding the rising phase. The oscillations were inhibited by the addition of 5μM nifedipine or the removal of extracellular Ca2+suggesting they are at least in part dependent on voltage gated Ca2+entry.
内皮素作用：蛋白激酶 C 抑制剂的抑制和磷酸肌醇的参与。
DOI：
10.1016/s0006-291x(89)80193-7
发表时间：
1989
影响因子：
3.1
作者：
Sugiura,M;Inagami,T;Hare,GM;Johns,JA
通讯作者：
Johns,JA