Increased rhythmicity in hypertensive arterial smooth muscle is linked to transient receptor potential canonical channels.
Increased rhythmicity in hypertensive arterial smooth muscle is linked to transient receptor potential canonical channels.
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高血压动脉平滑肌节律性的增加与瞬时受体电位经典通道有关。
DOI：
10.1111/j.1582-4934.2009.00890.x
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发表时间：
2010-10
影响因子：
5.3
通讯作者：
Zhu Z
中科院分区：
文献类型：
--
作者：
Chen X;Yang D;Ma S;He H;Luo Z;Feng X;Cao T;Ma L;Yan Z;Liu D;Tepel M;Zhu Z
血管运动描述了由于细胞内钙离子浓度的同步变化而引起的动脉血管张力的振荡。由于自发性高血压大鼠(SHR)血管平滑肌细胞钙内流增加与瞬时受体潜伏期(TRPC)通道的变化有关，在本研究中，我们验证了高血压时血管运动增加与TRPC表达增加直接相关的假说。使用小血管肌图仪，我们观察到与正常血压的Wistar-京都(WKY)大鼠相比，SHR的肠系膜小动脉由去甲肾上腺素引起的血管运动显着增加。免疫印迹法检测到SHR大鼠肠系膜小动脉中TRPC1、TRPC3和TRPC5的表达显著高于WKY，而TRPC4和TRPC6的表达无明显差异。在维拉帕米、SKF96365、2-氨基乙氧基二苯基硼烷(2-APB)或Gd存在下，去甲肾上腺素引起的SHR血管运动明显减弱。预先用抗TRPC1和抗TRPC3抗体孵育肠系膜小动脉可显著减少去甲肾上腺素引起的血管收缩和钙内流。与TRPC抗体及其相应抗原肽预先孵育的对照实验，或与抗β-肌动蛋白抗体或与TRPC通道无关的随机免疫球蛋白存在的对照实验表明，去甲肾上腺素诱导的血管运动和钙内流没有抑制作用。给SHR应用坎地沙坦或替米沙坦16周，但不给予氨氯地平，可显著降低TRPC1、TRPC3和TRPC5的表达以及去甲肾上腺素引起的肠系膜小动脉的血管运动。综上所述，我们提供的实验证据表明，自发性高血压大鼠肠系膜小动脉TRPC1、TRPC3和TRPC5表达增加，导致高血压时血管运动增强。
Vasomotion describes oscillations of arterial vascular tone due to synchronized changes of intracellular calcium concentrations. Since increased calcium influx into vascular smooth muscle cells from spontaneously hypertensive rats (SHR) has been associated with variances of transient receptor potential canonical (TRPC) channels, in the present study we tested the hypothesis that increased vasomotion in hypertension is directly linked to increased TRPC expression. Using a small vessel myograph we observed significantly increased norepinephrine-induced vasomotion in mesenteric arterioles from SHR compared to normotensive Wistar–Kyoto (WKY) rats. Using immunoblottings we obtained significantly increased expression of TRPC1, TRPC3 and TRPC5 in mesenteric arterioles from SHR compared to WKY, whereas TRPC4 and TRPC6 showed no differences. Norepinephrine-induced vasomotion from SHR was significantly reduced in the presence of verapamil, SKF96365, 2-aminoethoxydiphenylborane (2-APB) or gadolinium. Pre-incubation of mesenteric arterioles with anti-TRPC1 and anti-TRPC3 antibodies significantly reduced norepinephrine-induced vasomotion and calcium influx. Control experiments with pre-incubation of TRPC antibodies plus their respective antigenic peptide or in the presence of anti-β-actin antibodies or random immunoglobulins not related to TRPC channels showed no inhibitory effects of norepinephrine-induced vasomotion and calcium influx. Administration of candesartan or telmisartan, but not amlodipine to SHR for 16 weeks significantly reduced either the expression of TRPC1, TRPC3 and TRPC5 as well as norepinephrine-induced vasomotion in mesenteric arterioles. In conclusion we gave experimental evidence that the increased TRPC1, TRPC3 and TRPC5 expression in mesenteric arterioles from SHR causes increased vasomotion in hypertension.
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影响因子：
19.6
作者：
Fellner, SK;Arendshorst, WJ
通讯作者：
Arendshorst, WJ
影响因子：
15.9
作者：
HAJDUCZOK, G;CHAPLEAU, MW;ABBOUD, FM
通讯作者：
ABBOUD, FM
影响因子：
10.8
作者：
Huang, Y;Chan, FL;Yao, XQ
通讯作者：
Yao, XQ
影响因子：
8.3
作者：
Liu, Daoyan;Yang, Dachun;Tepel, Martin
通讯作者：
Tepel, Martin
影响因子：
20.1
作者：
Mather, S;Dora, KA;Garland, CJ
通讯作者：
Garland, CJ