Altered signal transduction in vascular smooth muscle cells of spontaneously hypertensive rats.
Altered signal transduction in vascular smooth muscle cells of spontaneously hypertensive rats.
复制标题
自发性高血压大鼠血管平滑肌细胞信号转导的改变。
DOI：
10.1161/01.hyp.19.2_suppl.ii142
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Bhalla,RC
中科院分区：
文献类型：
--
作者：
Bendhack,LM;Sharma,RV;Bhalla,RC
通过测定自发性高血压大鼠（SHR）血管平滑肌（VSM）细胞胞浆游离钙浓度（[Ca2+]i）的变化，验证了血小板衍生生长因子（PDGF）和血管紧张素II （Ang II）介导的信号转导发生改变的假设。采用fura-2作为钙离子指标和显微数字图像分析系统，测定了SHRs和Wistar-Kyoto （WKY）正常血压大鼠培养的主动脉平滑肌细胞中的[Ca2+]i。Ang II激活细胞导致[Ca2+]i迅速升高，尽管是短暂的；在间隔10-30秒后观察到最大的增加。另一方面，具有PDGF BB的细胞激活产生[Ca2+]i的增加，具有40-60秒的滞后期；添加PDGF后2 ~ 4分钟出现最大增幅。通过添加钙通道拮抗剂维拉帕米（100微米）以及从细胞外洗浴培养基中去除钙，pdgf刺激的[Ca2+]i的增加明显受到抑制。然而，添加维拉帕米或去除细胞外钙对Ang ii刺激的[Ca2+]i没有显著影响。这些结果表明，pdgf介导的VSM细胞中[Ca2+]i的增加主要是通过Ca2+内流，而Ang ii介导的增加是由于细胞内钙池的释放。与WKY细胞相比，SHR VSM细胞中基础的、PDGF-和Ang ii刺激的[Ca2+]i升高显著高于WKY细胞（p < 0.05）。（摘要删节250字）
The hypothesis that signal transduction mediated by platelet-derived growth factor (PDGF) and angiotensin II (Ang II) is altered in vascular smooth muscle (VSM) cells from the spontaneously hypertensive rat (SHR) was tested by measuring changes in the cytosolic free calcium concentration ([Ca2+]i). [Ca2+]i was measured in cultured aortic smooth muscle cells from SHRs and Wistar-Kyoto (WKY) normotensive rats using fura-2 as a calcium indicator and a microscopic digital image analysis system. Activation of cells with Ang II resulted in a prompt though transient rise in [Ca2+]i; the maximum increase was observed after 10-30-second intervals. On the other hand, activation of cells with PDGF BB produced an increase in [Ca2+]i with a 40-60-second lag period; the maximum increase was observed 2-4 minutes after the addition of PDGF. PDGF-stimulated increases in [Ca2+]i were markedly inhibited by the addition of the calcium channel antagonist verapamil (100 microM) as well as by removal of calcium from the extracellular bathing medium. However, Ang II-stimulated [Ca2+]i was not significantly affected by the addition of verapamil or by removal of extracellular calcium. These results would indicate that PDGF-mediated increases in [Ca2+]i in VSM cells are predominantly via Ca2+ influx, whereas Ang II-mediated increases are due to calcium release from intracellular pools. Basal and PDGF- and Ang II-stimulated increases in [Ca2+]i were significantly greater (p less than 0.05) in SHR VSM cells compared with WKY cells.(ABSTRACT TRUNCATED AT 250 WORDS)