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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Decreased inward rectifier and voltage-gated K+ currents of the right septal coronary artery smooth muscle cells in pulmonary arterial hypertensive rats
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Decreased inward rectifier and voltage-gated K+ currents of the right septal coronary artery smooth muscle cells in pulmonary arterial hypertensive rats

机译：肺动脉高血压大鼠右侧冠状动脉平滑肌细胞的向内整流器和电压门控K +电流降低

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In vascular smooth muscle, Ksup+/sup channels, such as voltage-gated Ksup+/sup channels (Kv), inward-rectifier Ksup+/sup channels (Kir), and big-conductance Casup2+/sup-activated Ksup+/sup channels (BKsubCa/sub), establish a hyperpolarized membrane potential and counterbalance the depolarizing vasoactive stimuli. Additionally, Kir mediates endothelium-dependent hyperpolarization and the active hyperemia response in various vessels, including the coronary artery. Pulmonary arterial hypertension (PAH) induces right ventricular hypertrophy (RVH), thereby elevating the risk of ischemia and right heart failure. Here, using the whole-cell patch-clamp technique, we compared Kv and Kir current densities (IsubKv/sub and IsubKir/sub) in the left (LCSMCs), right (RCSMCs), and septal branches of coronary smooth muscle cells (SCSMCs) from control and monocrotaline (MCT)-induced PAH rats exhibiting RVH. In control rats, (1) IsubKv/sub was larger in RCSMCs than that in SCSMCs and LCSMCs, (2) IsubKv/sub inactivation occurred at more negative voltages in SCSMCs than those in RCSMCs and LCSMCs, (3) IsubKir/sub was smaller in SCSMCs than that in RCSMCs and LCSMCs, and (4) IsubBKCa/sub did not differ between branches. Moreover, in PAH rats, IsubKir/sub and IsubKv/sub decreased in SCSMCs, but not in RCSMCs or LCSMCs, and IsubBKCa/sub did not change in any of the branches. These results demonstrated that SCSMC-specific decreases in IsubKv/sub and IsubKir/sub occur in an MCT-induced PAH model, thereby offering insights into the potential pathophysiological implications of coronary blood flow regulation in right heart disease. Furthermore, the relatively smaller IsubKir/sub in SCSMCs suggested a less effective vasodilatory response in the septal region to the moderate increase in extracellular Ksup+/sup concentration under increased activity of the myocardium.
机译：在血管平滑肌中，k + 通道，例如电压门控k + 通道（kv），向内整流k + 通道（Kir ）和大电导Ca 2 + -tivated k + 通道（Bk ca ），建立超极化的膜电位并抵消去极化vasoactive刺激。此外，KIR介导内皮依赖性的超极化和各种血管中的活性充血反应，包括冠状动脉。肺动脉高血压（PAH）诱导右心室肥大（RVH），从而提高缺血和右心力衰竭的风险。在这里，使用整个细胞补丁钳技术，我们比较了左侧（LCSMCS），右（RCSMC）中的KV和KIR电流密度（I KV 和I Kir ）（RCSMC ），来自对照的冠状动脉平滑肌细胞（SCSMC）的隔膜分支和偏相体（MCT）诱导的PAH大鼠表现出RVH。在对照大鼠中，（1）I kv 在rcsmcs中比在scsmcs和lcsmcs中更大，（2）I kv 失活在scsmcs中的更多负电压发生而不是那些RCSMCS和LCSMCS，（3）I kir 在scsmcs中较小，而不是rcsmcs和lcsmcs，并且（4）I bkca 分支之间没有区别。此外，在PAH大鼠中，I kir 和i kv 在scsmc中减少，但不是在rcsmcs或lcsmcs中，我 bkca 没有变化任何分支机构。这些结果表明，I kV 和I kir 在MCT引起的PAH模型中发生了SCSMC特异性降低，从而提供了冠状动脉血流调节的潜在病理生理学意义的见解在右心疾病中。此外，SCSMC中的相对较小的I Kir 在子宫内的细胞外k + 浓度下的温和血管区舒张响应较小，在心肌的增加下浓度较低。

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