Key result
TRPV1 knockout or chemical ablation of TRPV1-expressing cardiac afferents attenuated pressure overload-induced cardiac hypertrophy and BDNF increase in the nucleus tractus solitarius.
Why the study?
To investigate whether TRPV1-expressing cardiac afferent nerves contribute to cardiac hypertrophy accompanied by increased BDNF expression in the nucleus tractus solitarius.
Does TRPV1 knockout or ablation of TRPV1-expressing cardiac afferents attenuate pressure overload-induced cardiac hypertrophy and BDNF expression in the NTS in mice?
Does TRPV1 knockout or ablation of TRPV1-expressing cardiac afferents attenuate pressure overload-induced cardiac hypertrophy and BDNF expression in the NTS in mice?
TRPV1-expressing cardiac afferent nerves contribute to pressure overload-induced cardiac hypertrophy, accompanied by increased BDNF expression in the NTS.
Answers are grounded in this paper and cite their sources.
Should not yet change practice; leaves open TRPV1 cardiac afferents as a potential target in pressure-overload hypertrophy.
INTRODUCTION: Increased sympathetic output contributes to cardiac hypertrophy. Sympathoexcitation is induced by activating the cardiac sympathetic afferent nerves through transient receptor potential vanilloid 1 (TRPV1) in cardiac afferent endings. Brainstem nucleus tractus solitarius (NTS) receives the sensory cardiac afferent inputs. Brain-derived neurotrophic factor (BDNF) is released within NTS from sensory neurons in an activity-dependent manner. Additionally, BDNF in NTS tonically regulates sympathetic activity. Therefore, we hypothesized that TRPV1-expressing cardiac afferent nerves contribute to cardiac hypertrophy in accompany with an increased BDNF expression in NTS. METHODS AND RESULTS: Abdominal aortic banding (AB) or sham operation was conducted in wild-type C57BL/6 J (WT-AB) and TRPV1 knockout mice (TRPV1 KO-AB). At 8 weeks post-operation, echocardiographic left ventricular wall thickness and heart weight/body weight ratio were significantly greater in WT-AB than WT-Sham mice, and these hypertrophic indexes were attenuated in TRPV1 KO-AB mice. Among the groups, left ventricular fractional shortening was not different. The protein levels of TRPV1 in heart and BDNF in NTS were significantly increased in WT-AB compared to WT-Sham mice, whereas BDNF expression in NTS was not increased by AB in TRPV1-KO mice. Chemical ablation of TRPV1-expressing cardiac afferents attenuated the AB-induced cardiac hypertrophy and increase in BDNF in NTS. Sympathetic activity analyzed using heart rate variability, and sympathoexcitatory responses to the stimulation of cardiac afferents were increased in WT-AB compared to WT-Sham mice. CONCLUSION: TRPV1-expressing cardiac afferent nerves may contribute to pressure overload-induced cardiac hypertrophy in accompany with the increased BDNF within NTS.
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Shibata et al. (2022) studied Cardiac hypertrophy. TRPV1 knockout or chemical ablation vs. Wild-type / Sham was evaluated on Cardiac hypertrophy (left ventricular wall thickness and heart weight/body weight ratio). TRPV1 knockout or chemical ablation of TRPV1-expressing cardiac afferents attenuated pressure overload-induced cardiac hypertrophy and BDNF increase in the nucleus tractus solitarius.
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