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Effect of knockout of the ASIC3 on cardiovascular reflexes arising from hindlimb muscle in decerebrated rats

机译:ASIC3敲除对切颅大鼠后肢肌肉产生心血管反应的影响

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摘要

The exercise pressor reflex is initialed by the contraction-induced activation of group 111 and IV muscle afferents. The reflex is manifested by increases in arterial blood pressure and cardiac output, which, in turn, are generated by increases in the sympathetic outflow to the heart and vasculature and decreases in the vagal outflow to the heart. In previous experiments, we used a pharmacological approach to assess the role played by the acid-sensing ion channel 3 (AS1C3) on group III and IV afferents in evoking the exercise pressor reflex. In the present experiments, we used an alternative approach, namely functional knockout (KO) of the ASIC3 gene, to confirm and extend our previous finding that pharmacological blockade of the ASIC3 had only a small impact on the expression of the exercise pressor reflex when the arterial supply to the contracting hindlimb muscles of rats was patent. Using this alternative approach, we compared the magnitude of the exercise pressor reflex evoked in ASIC3 KO rats with that evoked in their wild-type (WT) counterparts.
机译:运动压力液反射由组111和IV肌事件的收缩诱导的激活来初始化。通过动脉血压和心脏输出的增加表现出反射,这反过来又产生了对心脏和脉管系统的同情流出的增加,并且缩小流出到心脏。在先前的实验中,我们使用了药理学方法来评估酸感测离子通道3(AS1C3)在III组和IV型传入中唤起运动压力机反射中的作用。在目前的实验中,我们使用了一种替代方法,即ASIC3基因的功能淘汰(KO),以确认并延长我们之前发现ASIC3的药理学封锁对运动压力机反射的表达仅对少量影响对大鼠合同后肢肌肉的动脉供应是专利。使用这种替代方法,我们比较了在野生型(WT)对应物中诱发ASIC3 KO大鼠中诱发的运动压力机反射的大小。

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