• Tao Zhang, Mamoru Tanida, Kunitoshi Uchida, Yoshiro Suzuki, Wei Yang, Yuhichi Kuda, Yasutaka Kurata, Makoto Tominaga, and Toshishige Shibamoto.
• *Department of Physiology II, Kanazawa Medical University, Uchinada, Japan †Department of Colorectal and Hernia Surgery, The Fourth Affiliated Hospital of China Medical University, Shenyang, China ‡Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), National Institutes of Natural Sciences, Okazaki, Japan §Department of Physiological Science and Molecular Biology, Fukuoka Dental College, Fukuoka, Japan ||Department of Infectious Disease, The Sheng Jing Hospital of China Medical University, Shenyang, China.
• Shock. 2017 Nov 1; 48 (5): 576-582.

AimThe inhibitory responses of renal sympathetic nerve activity (RSNA) and heart rate (HR) to sustained hemorrhagic shock occurred in anesthetized rats, but have not yet been determined in mice. Here, we investigated the responses of RSNA and HR to hemorrhagic hypotension in anesthetized mice, with an emphasis on the molecule-based mechanism for roles of afferent vagal nerves.MethodsRSNA, HR, and mean systemic arterial pressure were continuously measured in male pentobarbital-anesthetized C57BL/6N mice. Hemorrhagic hypotension of 50 mmHg was evoked and maintained for 10 min.ResultsDuring hemorrhagic hypotension, RSNA initially increased and then sustainedly decreased, while HR progressively decreased. Vagotomy eliminated the second-phase sympathoinhibition and bradycardia, and carotid sinus denervation with vagotomy abolished the initial renal sympathoexcitation. The renal sympathoinihibition during hemorrhagic hypotension of 50 mmHg was eliminated in mice pretreated with a transient receptor potential vanilloid type 1 channel (TRPV1) inhibitor, capsazepine, and in TRPV1 knockout (TRPV1) mice, but not in TRPV4 knockout mice. The bradycardia response to hemorrhagic hypotension was also absent in TRPV1 mice and mice pretreated with capsazepine.ConclusionHemorrhagic hypotension in anesthetized mice causes biphasic responses of RSNA with an initial increase, followed by a sustained decrease, and a progressive decrease in HR. The initial sympathoexcitation is mediated by carotid sinus baroreceptors, while the later sympathoinhibition and bradycardia are mediated via the TRPV1 signals of vagal afferents.

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