Background: Sympathetic hyperactivity plays a major role in the development and progression of cardiac hypertrophy. Augmented input from cardiac afferents can cause sympathoexcitation. In the brain, brain-derived neurotrophic factor (BDNF) can inhibit neuronal excitability in nucleus tractus solitarius (NTS) which receives cardiac afferent inputs, and consequently lead to sympathoexcitaion. We hypothesized that the cardiac afferent signaling may be enhanced via the activation of transient receptors potential vanilloid type 1 (TRPV1) in the cardiac afferent endings, and BDNF in NTS may be increased in cardiac hypertrophy. Methods and Results: Cardiac hypertrophy was induced by abdominal aortic banding (AAB) in male C57BL/6J mice. Western blotting showed that the expression of TRPV1 in heart and BDNF in NTS were increased in AAB-mice compared to sham-operated control mice (TRPV1: 1.44 ± 0.17 vs. 0.91 ± 0.04 units; BDNF: 1.35 ± 0.03 vs. 0.92 ± 0.02 units; n = 6 for each, P < .05). To evaluate the sympathoexcitatory pressor response elicited by cardiac afferent activation via heart-TRPV1, capsaicin (2.5 mM, 2 µl), a TRPV1 agonist, was applied to epicardium of left ventricle with measuring blood pressure. The pressor response was significantly greater in AAB-mice than controls (34.4 ± 4.0 vs. 17.7 ± 2.3 mmHg, n = 5–7, P < .05). These AAB-induced changes were attenuated in TRPV1-knockout mice (NTS-BDNF, 0.92 ± 0.05 units, n = 6; pressor response, 1.8 ± 3.1 mmHg, n = 2). Conclusion: Cardiac afferent nerve activation via heart-TRPV1 and increase of NTS-BDNF might be involved in sympathoexcitation in cardiac hypertrophy.
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