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首页> 外文期刊>Cellular Physiology and Biochemistry >Proteinase-Activated Receptor-2 Sensitivity of Amplified TRPA1 Activity in Skeletal Muscle Afferent Nerves and Exercise Pressor Reflex in Rats with Femoral Artery Occlusion
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Proteinase-Activated Receptor-2 Sensitivity of Amplified TRPA1 Activity in Skeletal Muscle Afferent Nerves and Exercise Pressor Reflex in Rats with Femoral Artery Occlusion

机译：股骨动脉阻塞大鼠骨骼肌传入神经中TRPA1活性的蛋白酶激活的受体2敏感性和运动加压反射。

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>Background/Aims: Limb ischemia occurs in peripheral artery disease (PAD). Sympathetic nerve activity (SNA) that regulates blood flow directed to the ischemic limb is exaggerated during exercise in this disease, and transient receptor potential channel A1 (TRPA1) in thin-fiber muscle afferents contributes to the amplified sympathetic response. The purpose of the present study was to determine the role of proteinase-activated receptor-2 (PAR2) in regulating abnormal TRPA1 function and the TRPA1-mediated sympathetic component of the exercise pressor reflex. Methods: A rat model of femoral artery ligation was employed to study PAD. Dorsal root ganglion (DRG) tissues were obtained to examine the protein levels of PAR2 using western blot analysis. Current responses induced by activation of TRPA1 in skeletal muscle DRG neurons were characterized using whole-cell patch clamp methods. The blood pressure response to static exercise (i.e., muscle contraction) and stimulation of TRPA1 was also examined after a blockade of PAR2. Results: The expression of PAR2 was amplified in DRG neurons of the occluded limb, and PAR2 activation with SL-NH2 (a PAR2 agonist) increased the amplitude of TRPA1 currents to a greater degree in DRG neurons of the occluded limb. Moreover, FSLLRY-NH2 (a PAR antagonist) injected into the arterial blood supply of the hindlimb muscles significantly attenuated the pressor response to muscle contraction and TRPA1 stimulation in rats with occluded limbs. Conclusions: The PAR2 signal in muscle sensory nerves contributes to the amplified exercise pressor reflex via TRPA1 mechanisms in rats with femoral artery ligation. These findings provide a pathophysiological basis for autonomic responses during exercise activity in PAD, which may potentially aid in the development of therapeutic approaches for improvement of blood flow in this disease.
机译：> 背景/目的： 肢体缺血发生在外周动脉疾病（PAD）中。在该疾病的运动过程中，调节定向到缺血肢体的血流的交感神经活动（SNA）被夸大了，并且细纤维肌肉传入的瞬时受体电位通道A1（TRPA1）促进了交感神经反应的放大。本研究的目的是确定蛋白酶激活受体2（PAR2）在调节TRPA1异常功能和运动加压反射中TRPA1介导的交感成分中的作用。 方法： 采用大鼠股动脉结扎模型研究PAD。使用蛋白质印迹分析获得背根神经节（DRG）组织以检查PAR2的蛋白质水平。使用全细胞膜片钳方法表征了骨骼肌DRG神经元中TRPA1激活引起的电流响应。阻断PAR2后，还要检查对静态运动（即肌肉收缩）和TRPA1刺激的血压反应。 结果： PAR2的表达在被闭塞的肢体的DRG神经元中被扩增，并且SL-NH2（PAR2激动剂）激活PAR2将TRPA1电流的幅度增加到了闭塞肢体的DRG神经元的程度更高。此外，将FSLLRY-NH2（一种PAR拮抗剂）注射到后肢肌肉的动脉血液中可显着减弱四肢闭塞的大鼠对肌肉收缩和TRPA1刺激的升压反应。 结论： 肌肉感觉神经中的PAR2信号通过TRPA1机制促进股动脉结扎大鼠的运动加压反射。这些发现为PAD运动过程中的自主神经反应提供了病理生理基础，这可能潜在地有助于开发改善该疾病血流的治疗方法。

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