CD4⁺T-cells expressing choline acetyltransferase (ChAT) have recently been shown to cause a drop in systemic blood pressure when infused into mice. The aim of this study was to determine if ChAT expressing T-cells could regulate coronary vascular reactivity. Pre-constricted segments of epicardial and intramyocardial porcine coronary arteries relaxed in response to Jurkat T-cells (JT) that overexpressed ChAT (JT_ChAT cells). The efficacy of the JT_ChAT cells was similar in epicardial and intramyocardial vessels with a maximum dilator response to 3x10⁵cells/mL of 38·0±6.7 and 38·7±7.25% respectively. In contrast, non-transfected JT cells elicited a weak dilator response, followed by a weak contraction. The response of JT_ChAT cells was dependent upon the presence of the endothelial cells. In addition, the response could be significantly reduced by L-NAME and ODQ in the presence of indomethacin. JT_ChAT cells, but not JT cells increased the expression of phosphorylated eNOS. JT_ChAT cells contained significantly greater levels of acetylcholine compared to JT cells, however, the non-selective muscarinic antagonist atropine and the M₁ receptor antagonist pirenzepine both failed to block the dilator effect of JT_ChAT cells. Exogenously added acetylcholine induced only a weak relaxation (_~10%) at low concentrations, which became a contractile response at higher concentrations. These data illustrate the capacity for cells that express ChAT to regulate coronary vascular reactivity, via mechanisms that are dependent upon interaction with the endothelium and in part mediated by the release of nitric oxide.

中文翻译：

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由表达胆碱乙酰转移酶的 T 细胞介导的冠状血管舒张

表达胆碱乙酰转移酶 (ChAT) 的CD4 ⁺ T 细胞最近被证明在注入小鼠时会导致全身血压下降。本研究的目的是确定表达 ChAT 的 T 细胞是否可以调节冠状血管反应性。猪冠状动脉的心外膜和心肌内预收缩段因过度表达 ChAT（JT _ChAT细胞）的Jurkat T 细胞（JT）而松弛。JT _ChAT细胞在心外膜和心肌内血管中的功效相似，对 3x10 ⁵细胞/mL 的最大扩张器反应分别为38·0±6.7 和 38·7±7.25%。相比之下，未转染的 JT 细胞引起微弱的扩张器反应，然后是微弱的收缩。JT _Chat的回应细胞依赖于内皮细胞的存在。此外，在存在吲哚美辛的情况下，L-NAME 和 ODQ 可显着降低响应。JT _ChAT细胞而不是 JT 细胞增加了磷酸化 eNOS 的表达。与 JT 细胞相比，JT _ChAT细胞含有显着更高水平的乙酰胆碱，然而，非选择性毒蕈碱拮抗剂阿托品和 M ₁受体拮抗剂哌仑西平均未能阻断 JT _ChAT细胞的扩张作用。外源性添加的乙酰胆碱仅诱导微弱的弛豫（_~10%) 在低浓度下，在较高浓度下变成收缩反应。这些数据说明了表达 ChAT 的细胞通过依赖于与内皮相互作用并部分由一氧化氮释放介导的机制来调节冠状血管反应性的能力。