Purinergic and adrenergic Ca2+ transients during neurogenic contractions of rat mesenteric small arteries
Purinergic and adrenergic Ca2+ transients during neurogenic contractions of rat mesenteric small arteries
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DOI：
10.1113/jphysiol.2003.043380
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发表时间：
2003-06-15
影响因子：
5.5
通讯作者：
Wier, WG
中科院分区：
文献类型：
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作者：
Lamont, C;Vainorius, E;Wier, WG
小动脉的收缩受交感神经系统调节，但完整小动脉神经刺激收缩期间的 Ca2+ 瞬变尚未被记录。我们将荧光 Ca2+ 指示剂 Fluo-4 装载到大鼠肠系膜小动脉中，并将其安装在肌动描记器中，该肌描记器可以同时对单个平滑肌细胞的荧光进行高速共聚焦成像，(ii) 血管周围神经的电刺激，以及 (iii) 记录等长张力。在辣椒素和东莨菪碱（分别抑制“感觉”和胆碱能神经）的情况下，通过电场刺激（EFS）（频率，10 Hz；脉冲电压，40 V；脉冲持续时间，0.2 ms）实现交感神经肌肉传递。在 EFS 的前 20 秒内，力上升至一个小峰值，然后下降。在此期间，交界 Ca2+ 瞬变 (jCaTs) 以相对较高的频率出现。我们之前将 jCaT 归因于 Ca2+ 通过 ATP 激活的连接后 P2X 受体流入。传播的异步 Ca2+ 波最初并不存在，以前与浴应用的 α(1)-肾上腺素受体激动剂相关。在接下来的 2.5 分钟 EFS 中，力缓慢上升，出现异步传播的 Ca2+ 波。选择性α(1)-肾上腺素受体拮抗剂哌唑嗪消除了缓慢发展的收缩和Ca2+波，但仅将初始短暂收缩减少了约25%。在哌唑嗪 EFS 3 分钟期间，jCaT 频率显着下降；在至少发生一次 jCaT 的部位，前 20 秒内发生 jCaT 的平均概率为 0.008 +/- 0.002 脉冲(-1)，后 20 秒内为 0.0007 +/- 0.0002 脉冲(-1)。我们认为，(i) 交感静脉曲张释放的 ATP 激活初始、短暂的收缩，并且激活剂 Ca 21 主要来自 jCaT，(ii) 交感神经释放的去甲肾上腺素 (NA) 通过涉及 α(1)-肾上腺素受体的机制激活后期的主要收缩，且与传播 Ca2+ 波相关。
Contraction of small arteries is regulated by the sympathetic nervous system, but the Ca2+ transients during neurally stimulated contraction of intact small arteries have not yet been recorded. We loaded rat mesenteric small arteries with the fluorescent Ca2+ indicator fluo-4 and mounted them in a myograph that permitted simultaneous (i) high-speed confocal imaging of fluorescence from individual smooth muscle cells, (ii) electrical stimulation of perivascular nerves, and (iii) recording of isometric tension. Sympathetic neuromuscular transmission was achieved by electrical field stimulation (EFS) (frequency, 10 Hz; pulse voltage, 40 V; pulse duration, 0.2 ms) in the presence of capsaicin and scopolamine (to inhibit 'sensory' and cholinergic nerves, respectively). During the first 20 s of EFS, force rose to a small peak and then declined. During this time, junctional Ca2+ transients (jCaTs) were present at relatively high frequency. We have previously attributed jCaTs to influx of Ca2+ through post-junctional P2X receptors activated by ATP. Propagating asynchronous Ca2+ waves, previously associated with bath-applied alpha(1)-adrenoceptor agonists, were not initially present. During the next 2.5 min of EFS, force rose slowly, and asynchronous propagating Ca2+ waves appeared. The selective alpha(1)-adrenoceptor antagonist prazosin abolished both the slowly developing contraction and the Ca2+ waves, but reduced the initial transient contraction by only similar to25 %. During 3 min of EFS in prazosin, the frequency of jCaTs declined markedly; at sites at which at least one jCaT occurred, the average probability of a jCaT was 0.008 +/- 0.002 pulse(-1) in the first 20 s and 0.0007 +/- 0.0002 pulse(-1) in the last 20 s. We suggest that (i) ATP released from sympathetic varicosities activates the initial, transient, contraction and the activator Ca 21 is derived largely from jCaTs, and (ii) sympathetically released noradrenaline (NA) activates the later, major contraction through mechanisms involving alpha(1)-adrenoceptors and which are associated with propagating Ca2+ waves.