Oral

[O2-E-PM2-03] Effects of the oral angiotensin-converting enzyme inhibitor captopril on occlusal-disharmony-induced cardiac dysfunction in mice

〇Aiko Ito¹, Yoshiki Ohnuki², Kenji Suita², Misao Ishikawa³, Ichiro Matsuo⁴, Yoshio Hayakawa⁵, Megumi Nariyama⁶, Hiroshi Tomonari¹, Satoshi Okumura² (1. Dept Orthodont, Tsurumi Univ Sch Dent Med, 2. Dept Physiol, Tsurumi Univ Sch Dent Med, 3. Dept Anat Histocyto, Tsurumi Univ Sch Dent Med, 4. Dept Periodont, Tsurumi Univ Sch Dent Med, 5. Dept Dent Anesthesiol, Tsurumi Univ Sch Dent Med, 6. Dept Pediatr Dent, Tsurumi Univ Sch Dent Med)

Keywords:筋組織、高次機能、シグナル伝達

Occlusal disharmony is known to affect not only oral cavity area but also autonomic nervous system in the heart. Since renin-angiotensin system (RAS) inhibitor captopril (Cap) is one of the first-line drugs for preventing cardiac remodeling in patients with heart failure, we hypothesized that Cpt might prevent cardiac dysfunction induced by occlusal disharmony. To test this hypothesis, we used a bite-opening (BO) mouse model, which was developed by cementing a suitable appliance onto the mandibular incisor. Mice (16-week, male C57BL/6) were divided into four groups: 1) Control, 2) BO, 3) Cap (via drinking water containing 0.1g/L), and 4) Cap + BO. After 2 weeks, cardiac function was significantly decreased with increased cardiac fibrosis and myocyte apoptosis in the BO group, compared to the control, and these changes were suppressed by Cap. We examined the mechanism and confirmed that cardiac dysfunction induced by BO was associated with dual phosphorylation on PKCδ (Tyr-311/Thr-505), leading to activation of CaMKII with increased phosphorylation of RyR2 and phospholamban. These results suggest that activation of RAS might play an important role for the development of cardiac diseases induced by occlusal anomalies.