Mouse Anaphylactic Hypotension Is Characterized by Initial Baroreflex Independent Renal Sympathoinhibition Followed by Sustained Renal Sympathoexcitation.

Mouse Anaphylactic Hypotension Is Characterized by Initial Baroreflex Independent Renal Sympathoinhibition Followed by Sustained Renal Sympathoexcitation.
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DOI:
10.3389/fphys.2017.00669
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发表时间:
2017
影响因子:
4
通讯作者:
Shibamoto T
Shibamoto T
中科院分区:
医学2区
文献类型:
--
作者:
Zhang T;Tanida M;Uchida K;Suzuki Y;Yang W;Kuda Y;Kurata Y;Tominaga M;Shibamoto T

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目的:小鼠全身过敏反应的血流动力学反应的特点是初始高血压,随后持续低血压。然而,交感神经系统对这种循环障碍的防御机制尚不清楚。在这里,我们研究了肾交感神经活动(RSNA)的反应,小鼠全身过敏反应,沿着的作用,颈动脉窦压力感受器,迷走神经和瞬时受体电位香草酸1型通道(TRPV 1)。方法:卵蛋白致敏的雄性C57 BL/6 N小鼠在戊巴比妥麻醉下使用。在抗原注射后60 min连续测量RSNA、体循环动脉压(SAP)和心率(HR)。结果:注射抗原后3 min内,RSNA沿着SAP的一过性升高而降低。此后,RSNA在持续性低血压期间显示进行性增加。相反,HR不断增加。窦主动脉去神经,但不迷走神经切断术,显着衰减肾交感神经兴奋和心动过速,分别从30和46分钟后,抗原。RSNA,SAP和HR对过敏反应的反应不受TRPV 1抑制剂辣椒平预处理或TRPV 1基因敲除的影响。结论:小鼠全身过敏反应引起双相RSNA反应,初始压力感受性反射非依赖性降低和继发性增加。晚期抗原诱导的交感兴奋和心动过速部分由颈动脉窦压力感受器介导。迷走神经和TRPV 1在麻醉小鼠的RSNA和HR反应中均不起作用。
Aim: The hemodynamic response to mouse systemic anaphylaxis is characterized by an initial hypertension followed by sustained hypotension. However, the defense mechanisms of the sympathetic nervous system against this circulatory disturbance is not known. Here, we investigated the renal sympathetic nerve activity (RSNA) response to mouse systemic anaphylaxis, along with the roles of carotid sinus baroreceptor, vagal nerves and the transient receptor potential vanilloid type 1 channel (TRPV1). Methods: Male ovalbumin-sensitized C57BL/6N mice were used under pentobarbital anesthesia. RSNA, systemic arterial pressure (SAP) and heart rate (HR) were continuously measured for 60 min after the antigen injection. Results: Within 3 min after antigen injection, RSNA decreased along with a transient increase in SAP. Thereafter, RSNA showed a progressive increase during sustained hypotension. In contrast, HR continuously increased. Sinoaortic denervation, but not vagotomy, significantly attenuated the renal sympathoexcitation and tachycardia from 30 and 46 min, respectively, after antigen. The responses of RSNA, SAP and HR to anaphylaxis were not affected by pretreatment with a TRPV1 inhibitor, capsazepine, or by genetic knockout of TRPV1. Conclusion: The mouse systemic anaphylaxis causes a biphasic RSNA response with an initial baroreflex-independent decrease and secondary increase. The antigen-induced sympathoexcitation and tachycardia at the late stage are partly mediated by carotid sinus baroreceptors. Either vagal nerve or TRPV1 does not play any significant roles in the RSNA and HR responses in anesthetized mice.
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