Cyclosporine Attenuates Pressure-Overload Hypertrophy in Mice While Enhancing Susceptibility to Decompensation and Heart Failure

• Published in: Circulation research 1999-04, Vol.84 (6), p.735-740
• Main Authors: Meguro, Tomomi, Hong, Chull, Asai, Kuniya, Takagi, Gen, McKinsey, Timothy A, Olson, Eric N, Vatner, Stephen F
• Format: Article
• Language: English
• Subjects: Animals; Aorta - physiology; Aorta, Abdominal - physiology; Aorta, Thoracic - physiology; Biological and medical sciences; Cardiovascular system; Cyclosporine - blood; Cyclosporine - pharmacology; Disease Susceptibility; Enzyme Inhibitors - blood; Enzyme Inhibitors - pharmacology; Heart Failure - etiology; Heart Failure - mortality; Heart Failure - physiopathology; Hypertension - mortality; Hypertension - physiopathology; Hypertrophy, Left Ventricular - mortality; Hypertrophy, Left Ventricular - pathology; Hypertrophy, Left Ventricular - physiopathology; Ligation; Male; Medical sciences; Mice; Pharmacology. Drug treatments; Vascular wall
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.res.84.6.735

Left ventricular hypertrophy (LVH) is a compensatory mechanism to cope with pressure overload. Recently, a calcineurin pathway mediating LVH and its prevention by cyclosporine was reported. We examined whether calcineurin mediates LVH due to pressure overload in mice. Pressure overload was induced by aortic banding in 53 mice (32 treated with cyclosporine [25 mg [middle dot] kg [middle dot] d], 21 treated with vehicle). There were 17 sham-operated mice (9 treated with vehicle, 8 treated with cyclosporine). At 3 weeks after surgery, LV weight to body weight was greater in the nontreatment banded group (4.39 +/- 0.16 mg/g) than in the cyclosporine-treated banded group (3.95 +/- 0.14 mg/g, P