Purpose: Hypertension promotes cardiac hypertrophy leading to Heart failure. Although aberrant mitochondrial dynamics is known to contribute to the pathogenesis of heart disease, little is known about the pathophysiological roles of Drp1, a mitochondrial fission protein, on the hypertensive cardiac hypertrophy. Methods and Results: Dahl salt sensitive rats (7 weeks) were started to feed with a chow containing low salt (0.3%: LS-group, n = 8) or high salt (8%: HS-group, n = 8) to induce hypertension. After 9 weeks, HS-group exhibited hypertension (systolic BP: 179.3 ± 8.9 mmHg, P < .01 vs 120.6 ± 4.8 mmHg of LS-group) and cardiac hypertrophy (heart weight/body weight: 0.5 ± 0.02% vs 0.35 ± 0.05%, P < .01). In the histologic analysis, HS-group revealed cardiac hypertrophy (Muscle fiber area: 795 ± 133 µm2, P < .05 vs 305.8 ± 39.5 µm2 of LS-group) and increased fibrosis (fibrotic area in azan staining: 34%, P < .05 vs 20% of LS-group). HS-group showed an increased expression in Drp1, whereas not significant in other mitochondrial dynamics proteins. In HS-group, when mdivi1 (an inhibitor of Drp1) was administered to rats (1 mg/kg by intraperitoneal injection every alternative day), the cardiac hypertrophy was suppressed (heart weight/body weight: 0.4 ± 0.0% with mdivi1, P < .01 vs 0.5 ± 0.02% without mdivi1) without alteration in BP. Conclusion: The myocardial Drp1-expression may be related to the pathogenesis of hypertensive cardiac hypertrophy.
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