Properties of synchronous spontaneous Ca2+ transients in the mural cells of rat rectal arterioles.
Properties of synchronous spontaneous Ca2+ transients in the mural cells of rat rectal arterioles.
复制标题
大鼠直肠小动脉壁细胞同步自发 Ca2 瞬变的特性。
DOI：
10.1007/s00424-017-1978-y
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发表时间：
2017
影响因子：
4.5
通讯作者：
Hashitani H.
中科院分区：
文献类型：
--
作者：
Mitsui R;Hashitani H.
内脏器官微静脉壁细胞（平滑肌细胞和周细胞）之间自发Ca 2+瞬变的同步性依赖于L型电压依赖性Ca 2+通道（LVDCC）依赖性去极化的细胞间扩散。然而，小动脉壁细胞之间自发性Ca 2+瞬变的同步性机制还不太清楚。通过Cal-520钙离子成像观察大鼠直肠粘膜下层小动脉壁细胞自发性胞内钙离子动态，分析其同步性。壁细胞细动脉，有一个圆形的细胞体与几个扩展的过程开发自发的“同步”钙瞬变所产生的Ca 2+释放肌内质网Ca 2+商店。间隙连接阻断剂（3 μM甘珀酸、10 μM 18β-大黄酸）、Ca 2+激活的Cl−通道（CaCC）阻断剂（100 μM 4，4 ′-二异硫氰酸芪-2，2 ′-二磺酸）或降低细胞外Cl−浓度（从134.4 mM降至12.4 mM）破坏了小动脉壁细胞之间Ca 2+瞬变的同步性。T型电压依赖性钙通道阻滞剂（TVDCCs，1 μM米贝拉地尔或ML 218）或LVDCCs（1 μM硝苯地平）分别降低钙瞬变频率或其曲线下面积（AUC）。然而，TVDCC和LVDCC阻断剂都不能破坏小动脉壁细胞间钙瞬变的同步性。这与硝苯地平破坏自发性Ca 2+瞬变同步的直肠小静脉相反。因此，由CaCC开放引起的自发瞬时去极化可以通过间隙连接有效地传播到相邻的小动脉壁细胞，以维持Ca 2+瞬时同步。TVDCCs的激活似乎加速自发性Ca 2+瞬变，而LVDCCs主要有助于Ca 2+瞬变的持续时间。
Synchrony of spontaneous Ca2+transients among venular mural cells (smooth muscle cells and pericytes) in visceral organs relies on the intercellular spread of L-type voltage-dependent Ca2+channel (LVDCC)-dependent depolarisations. However, the mechanisms underlying the synchrony of spontaneous Ca2+transients between arteriolar mural cells are less understood. The spontaneous intracellular Ca2+dynamics of arteriolar mural cells in the rat rectal submucosa were visualised by Cal-520 Ca2+imaging to analyse their synchrony. The mural cells in fine arterioles that had a rounded cell body with several extended processes developed spontaneous ‘synchronous’ Ca2+transients arising from Ca2+released from sarcoendoplasmic reticulum Ca2+stores. Gap junction blockers (3 μM carbenoxolone, 10 μM 18β-glycyrrhetinic acid), a Ca2+-activated Cl−channel (CaCC) blocker (100 μM 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid) or lowering extracellular Cl−concentration (from 134.4 to 12.4 mM) disrupted the synchrony of Ca2+transients between arteriolar mural cells. Blockers of T-type voltage-dependent Ca2+channels (TVDCCs, 1 μM mibefradil or ML218) or LVDCCs (1 μM nifedipine) reduced the Ca2+transient frequency or their area under curve (AUC), respectively. However, neither TVDCC nor LVDCC blockers disrupted the synchrony of Ca2+transients among arteriolar mural cells. This is in contrast with rectal venules in which nifedipine disrupted the synchrony of spontaneous Ca2+transients. Thus, spontaneous transient depolarisations arising from the opening of CaCCs may effectively spread to neighbouring arteriolar mural cells via gap junctions to maintain the Ca2+transient synchrony. Activation of TVDCCs appears to accelerate spontaneous Ca2+transients, while LVDCCs predominantly contribute to the duration of Ca2+transients.