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.
OBJECTIVE
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).


RESULTS
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, transforming growth 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.
Department of Cardiology, Nihon University Surugadai Hospital Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan. ii28181@yb3.so-net.ne.jp
Shinsuke
S
Harasawa
Yuji
Y
Otsuka
Katsuaki
K
Okubo
Miyuki
M
Koike
Hirotaka
H
Fujita
Toshio
T
Kushiro
Ken
K
Nagao
Atsushi
A
Hirayama
D000450:Aldosterone / Q000097:blood; D017311:Amlodipine / Q000494:pharmacology*; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D000959:Antihypertensive Agents / Q000378:metabolism / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002316:Cardiotonic Agents / Q000494:pharmacology*; D005353:Fibronectins / Q000235:genetics* / Q000378:metabolism; D005786:Gene Expression Regulation / Q000187:drug effects; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006973:Hypertension / Q000188:drug therapy* / Q000235:genetics / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D020097:Natriuretic Peptide, Brain / Q000235:genetics* / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000187:drug effects; D016212:Transforming Growth Factor beta / Q000235:genetics* / Q000378:metabolism
D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D002316:Cardiotonic Agents; D005353:Fibronectins; D016212:Transforming Growth Factor beta; D000804:Angiotensin II; D020097:Natriuretic Peptide, Brain; D017311:Amlodipine; D000450:Aldosterone; D012083:Renin