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首页> 外文期刊>BMC Physiology >Contribution of transient and sustained calcium influx, and sensitization to depolarization-induced contractions of the intact mouse aorta
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Contribution of transient and sustained calcium influx, and sensitization to depolarization-induced contractions of the intact mouse aorta

机译：瞬时和持续钙内流的贡献以及对去极化诱导的完整小鼠主动脉收缩的敏感性

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Background Electrophysiological studies of L-type Ca2+ channels in isolated vascular smooth muscle cells revealed that depolarization of these cells evoked a transient and a time-independent Ca2+ current. The sustained, non-inactivating current occurred at voltages where voltage-dependent activation and inactivation overlapped (voltage window) and its contribution to basal tone or active tension in larger multicellular blood vessel preparations is unknown at present. This study investigated whether window Ca2+ influx affects isometric contraction of multicellular C57Bl6 mouse aortic segments. Results Intracellular Ca2+ (Cai2+, Fura-2), membrane potential and isometric force were measured in aortic segments, which were clamped at fixed membrane potentials by increasing extracellular K+ concentrations. K+ above 20?mM evoked biphasic contractions, which were not affected by inhibition of IP3- or Ca2+ induced Ca2+ release with 2-aminoethoxydiphenyl borate or ryanodine, respectively, ruling out the contribution of intracellular Ca2+ release. The fast force component paralleled Cai2+ increase, but the slow contraction coincided with Cai2+ decrease. In the absence of extracellular Ca2+, basal tension and Cai2+ declined, and depolarization failed to evoke Cai2+ signals or contraction. Subsequent re-introduction of external Ca2+ elicited only slow contractions, which were now matched by Cai2+ increase. After Cai2+ attained steady-state, isometric force kept increasing due to Ca2+- sensitization of the contractile elements. The slow force responses displayed a bell-shaped voltage-dependence, were suppressed by hyperpolarization with levcromakalim, and enhanced by an agonist of L-type Ca2+ channels (BAY K8644). Conclusion The isometric response of mouse aortic segments to depolarization consists of a fast, transient contraction paralleled by a transient Ca2+ influx via Ca2+ channels which completely inactivate. Ca2+ channels, which did not completely inactivate during the depolarization, initiated a second, sustained phase of contraction, which was matched by a sustained non-inactivating window Ca2+ influx. Together with sensitization, this window L-type Ca2+ influx is a major determinant of basal and active tension of mouse aortic smooth muscle.
机译：背景技术在离体的血管平滑肌细胞中，L型Ca 2 + 通道的电生理研究表明，这些细胞的去极化作用引起了瞬时的和时间独立的Ca 2 + 电流。持续的非灭活电流出现在电压依赖性激活和灭活重叠（电压窗口）的电压上，目前尚不清楚其对较大的多细胞血管制剂中的基音或活动张力的作用。这项研究调查窗口Ca 2 + 流入是否影响多细胞C57Bl6小鼠主动脉节段的等距收缩。结果在主动脉段测量细胞内Ca 2 + （Ca i 2 + ，Fura-2），膜电位和等轴测力。通过增加细胞外K + 浓度将其固定在固定的膜电位上。超过20？mM的K + 引起双相收缩，不受IP 3 -或Ca 2 + 诱导的Ca 抑制的影响分别用2-氨基乙氧基二苯基硼酸酯或ryanodine释放2 + ，排除了细胞内Ca 2 + 释放的作用。平行于Ca i 2 + 的快速分力增加，但缓慢收缩与Ca i 2 + 的减少一致。在缺少细胞外Ca 2 + 的情况下，基础张力和Ca i 2 + 下降，去极化未能引起Ca i < / sub> 2 + 信号或收缩。随后重新引入外部Ca 2 + 只会引起缓慢的收缩，现在收缩与Ca i 2 + 的增加相匹配。 Ca i 2 + 达到稳态后，由于Ca 2 + -对收缩元素的敏化作用，等轴测力不断增大。缓慢的力响应呈现出钟形的电压依赖性，并被左旋克马卡林超极化抑制，并被L型Ca 2 + 通道的激动剂（BAY K8644）增强。结论小鼠主动脉节段对去极化的等距响应包括快速，短暂的收缩，并伴随Ca 2 + 通过Ca 2 + 通道完全失活流入。在去极化过程中并未完全失活的Ca 2 + 通道启动了第二个持续的收缩阶段，与持续的非失活窗口Ca 2 + 相匹配涌入。与敏化作用一起，该窗口L型Ca 2 + 大量涌入是小鼠主动脉平滑肌基础和活动张力的主要决定因素。

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