Amlodipine suppressed cardiac gene expression of brain natriuretic peptide, transforming growth factor-β1 and fibronectin mediated by aldosterone in male stroke-prone spontaneously hypertensive rats

Abstract

Abstract Objectives Amlodipine, a calcium channel blocker (CCB), is one of the most common antihypertensive medicines in Japan. We evaluated whether the calcium channel blocker confers cardiac protection through the renin–angiotensin–aldosterone system in male stroke-prone spontaneously hypertensive rats (SHR-SP). Methods Fifteen week-old rats were divided into 2 groups: amlodipine group (3 mg/kg/day, n = 5) and control group (n = 5). Key findings The CCB lowered systolic blood pressure significantly (P < 0.05). Plasma aldosterone concentration in the amlodipine group was remarkably lower than in the control group (P < 0.05), but plasma renin activity and plasma angiotensin II concentration were not different between the two groups. The CCB also suppressed the mRNA expression of brain natriuretic peptide, transforminggrowth factor-β1, and fibronectin extracted from the left ventricle. Conclusions These results suggest that amlodipine attenuates cardiac damage by lowering plasma aldosterone concentration in hypertensive rats with developing arteriosclerosis.