Hypertension is a chronic medical condition and a common complication of metabolic abnormalities in the cardiovascular system and is a major global health concern (He et al., 2016; do Carmo et al., 2016; Shih et al., 2016). Particularly, in the Frigid Zone, the incidence of secondary hypertension is more common compared with other warmer region. For instance, the north-east part of China, which is the coldest region in the country and the prevalent rate of hypertension is significantly higher (Pan Zhenwei et al., 2021) due mainly to the cold weather and diet habits (high salt and high fat) that are the known risk factors to cause the potential damage of kidney and metabolic disorder. It is well documented that high salt diet increases blood pressure (BP) via brain derived neurotrophic factor (BDNF)-mediated down-regulation of KCC2 and impaired baroreflex (BRx) inhibition of vasopressin neurons leading to vasoconstriction (Balapattabi et al., 2018; Prager-Khoutorsky et al., 2017; Choe et al., 2015). Recent findings have shown that BDNF gene plays a crucial role in thermogenesis control and energy expenditure (Wang et al., 2020; You et al., 2020; Colitti and Montanari, 2020). These findings may well explain the higher incidence of hypertension in the Frigid Zone. BDNF is a 247-amino acid diametric protein encoded by 1.45- and 3.5-kb messages that is widely distributed in the central nervous system (Ozcelik et al., 1991). Several lines of evidence have shown that BDNF mRNA expression within the para-ventricular nucleus of hypothalamus (PVN) is reported to increase in response to stimuli that are associated with elevations of BP, heart rate and mediate the cardiovascular stress response of angiotensin in PVN (Erdos et al., 2015). Micro-injection of BDNF into the rat medial NTS (mNTS), a region critical for baroreflex control of sympathetic outflow, produced dose-dependent increases in mean arterial pressure (MAP), heart rate (HR), and lumbar sympathetic nerve activity (LSNA) that were blocked by the tyrosine kinase inhibitor K252a (Clark et al., 2011). Additionally, BDNF has been shown to exert hypertensive actions in the brain-stem (Erdos et al., 2015; Wang and Zhou, 2002), however, it remains to be investigated whether BDNF-mediated depressor response by direct activation of baroreceptor at aorta through a reflex mechanism. Research has shown that BDNF-TrkB (Yousuf et al., 2019; Ortiz et al., 2018) are highly expressed and released in the nodose ganglia (NG), rostral ventrolateral medulla and in the nucleus tractus solitarius (NTS) (Wang and Zhou, 2002; Martin et al., 2009; Hsieh et al., 2010), the principal target of cardiovascular primary afferent inputs to the brainstem. All these results have pointed out that BNDF may play an opposite role in the regulation of BP via central (NTS) or peripheral mechanism, the BRx function (Shan et al., 2013; Becker et al., 2016; Liu et al., 2016; Vermehren-Schmaedick et al., 2013). In order to explore the direct role on baroreceptor, BDNF was applied by direct microinjection into the NG, i.e. direct activation of the cell body of the 1st-order of baroreceptor neurons (BRNs) in the NG. The current observation provides the first line of evidence that BDNF/TrkB expression in the NG is the key to activating baroreceptor and triggering the depressor response via BRx afferent function under both physiological and pathophysiological conditions, which indicates that BDNF by NTS administration indeed plays an exactly opposite role in autonomic control of BP regulation. This data definitely extends our understanding of the complicated physiological action of BDNF-TrkB signaling and may re-direct our research focus on an etiology of hypertension developed in the Frigid Zone.