Telmisartan predominantly suppresses cardiac fibrosis, rather than hypertrophy, in renovascular hypertensive rats.

Angiotensin II receptor blockers have beneficial effects in patients with cardiac diseases. We examined the effects of an angiotensin II receptor blocker, telmisartan, on cardiac remodeling in renovascular hypertensive rats. Telmisartan was administered to renovascular hypertensive rats at either a high dose (5 mg per kg per day; high-T group) or a low dose (0.5 mg per kg per day; low-T group). After 4 weeks, histomorphological studies, including an evaluation of cardiac fibrosis, hypertrophy, vascular changes and measurement of the serum aldosterone concentration, were performed. A significant reduction in systolic blood pressure was obtained in the high-T group, and the heart weight to body weight ratio in the high-T and low-T groups was significantly lower than that in the control renovascular hypertensive group. Cardiac and perivascular fibrosis and the accumulation of collagen were significantly suppressed in the high-T and low-T groups. An increase in the cross-sectional area of the myocytes and vessel hypertrophy were significantly prevented in the high-T group, but not in the low-T group. The dependence of myocyte lengthening on the blood pressure was also prevented in the high-T group, but not to a significant degree. The elevation of the serum aldosterone level observed in the renovascular hypertensive group was prevented in both the high-T and low-T groups.Treatment with telmisartan strongly suppresses the progression of cardiac fibrosis, rather than cardiac hypertrophy, in a manner that is independent of the blood pressure.