Participation of intracellular Ca2+ stores in arteriolar conducted responses.
Participation of intracellular Ca2+ stores in arteriolar conducted responses.
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DOI：
10.1152/ajpheart.00662.2002
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发表时间：
2003-07
期刊：
影响因子：
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通讯作者：
Y. Yashiro;B. Duling
中科院分区：
文献类型：
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作者：
Y. Yashiro;B. Duling
我们研究了细胞内钙储存在苯肾上腺素(PE)诱导的血管舒缩反应中所起的作用。当使用压力脉冲从微吸管射出的方法将PE短暂地(约1 S)作用于分离的中空小动脉时，PE产生强烈的局部血管收缩和非常小的双相传导反应(先小收缩后扩张)，并沿血管长度传播数百微米。用钙离子指示剂Fura 2测定，传导血管运动与刺激部位内皮细胞内钙离子浓度([Ca+]i)单相升高有关。钙泵抑制剂thapsigargin用于限制血管内皮细胞和血管内皮细胞的钙充盈。Thapsigarin减少了基线直径，并在局部部位引发了强烈的扩张器成分，同时增强了PE诱导的传导反应中的收缩和扩张器成分。腔外应用四乙基铵或轮藻毒素可模拟thapsigargin引起的增强传导收缩成分，但不能被伊贝毒素、阿帕明、格列本脲、钡或4-氨基吡啶所模拟。Thapsigargin使估计的基础内皮细胞[Ca~(2+)]i增加约60 nM，并将PE诱导的[Ca~(2+)]i变化从单相转变为双相，后期[Ca~(2+)]i高于基线，这与传导反应中增加的扩张性成分相一致。腔内应用河豚毒素和阿帕明可显著降低传导反应的舒张性成分。这些结果表明，在两种细胞中，细胞内钙库明显通过对KCA通道的调节而对传导的血管收缩反应起到动态调节作用。
We examined the role played by intracellular Ca2+ stores in conducted vasomotor responses induced by phenylephrine (PE) in isolated hamster cremasteric arterioles. When applied briefly ( approximately 1 s) to isolated, cannulated arterioles by using pressure-pulse ejection from a micropipette, PE produced a strong local vasoconstriction and a very small biphasic conducted response (a small constriction followed by a dilation) that propagated several hundred micrometers along the vessel length. The conducted vasomotion was associated with a monophasic elevation of the endothelial cell intracellular Ca2+ concentration ([Ca2+]i) at the site of stimulation, as measured with the Ca2+ indicator fura 2. The Ca2+ pump inhibitor thapsigargin was used to limit filling of Ca2+ stores in smooth muscle and endothelial cells. Thapsigargin reduced baseline diameter and elicited a strong dilator component at the local site while enhancing both the constrictor and dilator components of the PE-induced conducted response. The enhanced conducted constrictor component induced by thapsigargin was mimicked by extraluminal application of tetraethylammonium or charybdotoxin but not by iberiotoxin, apamin, glibenclamide, barium, or 4-aminopirydine. Thapsigargin increased the estimated basal endothelial cell [Ca2+]i by approximately 60 nM and converted the PE-induced change in [Ca2+]i from monotonic to biphasic with a late elevation of [Ca2+]i above baseline that coincided with the increased dilatory component of the conducted response. Luminal application of charybdotoxin plus apamin significantly reduced the dilatory component of the conducted response. These results indicate that intracellular Ca2+ stores play a dynamic role in regulating conducted vasomotor responses apparently through modulation of KCa channels in both cell types.