4.4 Article

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

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JOURNAL OF PHARMACY AND PHARMACOLOGY
卷 62, 期 12, 页码 1740-1745

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WILEY
DOI: 10.1111/j.2042-7158.2010.01164.x

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aldosterone; amlodipine; cardiac gene expression; fibronectin; SHR-SP

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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-beta(1), 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.

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