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Mechanisms of the thapsigargin-induced Ca2+ entry in in situ endothelial cells of the porcine aortic valve and the endothelium-dependent relaxation in the porcine coronary artery

机译:thapsigargin诱导猪主动脉瓣原位内皮细胞中Ca2 +进入的机制以及猪冠状动脉中内皮依赖性舒张

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摘要

The mechanisms of the thapsigargin (TG)-induced capacitative Ca2+ entry in in situ endothelial cells and its role in the regulation of arterial tone were investigated using front-surface fluorimetry and fura-2-loaded strips of porcine aortic valve and coronary artery.In the presence of extracellular Ca2+, TG induced an initial rapid and a subsequent sustained elevation of cytosolic Ca2+ concentration ([Ca2+]i) in valvular strips. In the absence of extracellular Ca2+, TG induced only a transient increase in [Ca2+]i.The TG-induced sustained elevation of [Ca2+]i in endothelial cells was inhibited completely by 1 mM Ni2+ and partly by 10 μM econazole and 30 μM ML-9, but not by 900 ng ml−1 pertussis toxin or 100 μM wortmannin. Therefore, cytochrome P450 and protein phosphorylation are suggested to be involved in the TG-induced Ca2+ influx in in situ endothelial cells.TG induced an endothelium-dependent large relaxation consisting of an initial and a late sustained relaxation in coronary arterial strip precontracted with U46619 (a thromboxane A2 analogue). Indomethacin alone had no effect, while indomethacin plus Nω-nitro-L-arginine (L-NOARG) markedly inhibited the sustained phase and slightly inhibited the initial phase of the TG-induced relaxation.TG induced a smaller but sustained relaxation during the 40 mM K+-induced precontraction than that seen during the U46619-induced precontraction. This relaxation was completely abolished by the pretreatment with indomethacin plus L-NOARG.In conclusion, both nitric oxide (NO) and endothelium-derived hyperpolarizing factor were suggested to mediate the TG-induced relaxation, while NO plays a major role in the sustained relaxation. The TG-induced sustained [Ca2+]i elevation in endothelial cells was thus suggested to be mainly linked to the sustained production of NO.
机译:使用前表面荧光法和呋喃2负载的猪主动脉瓣和冠状动脉条带,研究了毒胡萝卜素(TG)诱导的Ca2 +进入原位内皮细胞的机制及其在调节动脉张力中的作用。由于细胞外Ca2 +的存在,TG诱导了瓣膜条中胞质Ca2 +浓度([Ca2 +] i)的最初快速升高,随后持续升高。在不存在细胞外Ca2 +的情况下,TG仅诱导[Ca2 +] i瞬时增加。TG诱导的内皮细胞[Ca2 +] i持续升高被1 mM Ni2 +完全抑制,部分被10μM益康唑和30μMML抑制。 -9,但不是900μg/ ml-1百日咳毒素或100μm渥曼青霉素。因此,建议细胞色素P450和蛋白磷酸化参与TG诱导的原位内皮细胞Ca2 +内流.TG诱导内皮依赖性的大舒张,包括预先与U46619预收缩的冠状动脉条的初始和晚期持续舒张(血栓烷A2类似物)。单独的吲哚美辛没有作用,而吲哚美辛加Nω-硝基-L-精氨酸(L-NOARG)则显着抑制了TG诱导的松弛的持续阶段,并稍微抑制了初始阶段.TG在40μmM期间诱导了较小但持续的松弛K +引起的预收缩比U46619引起的预收缩。吲哚美辛加L-NOARG预处理完全消除了这种松弛现象。总之,建议一氧化氮(NO)和内皮衍生的超极化因子介导TG诱导的松弛,而NO在持续松弛中起主要作用。因此,TG诱导的内皮细胞持续的[Ca2 +] i升高主要与NO的持续产生有关。

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