Antihypertrophic effect of dihydropyridines calcium channel blockers is dependent on their potential of blocking N-type calcium channel.
- Author:
Qiong LUO
1
;
Wan-ling XUAN
;
Fang XI
;
Yu-lin LIAO
;
Masafumi KITAKAZE
Author Information
- Publication Type:Journal Article
- MeSH: Amlodipine; pharmacology; therapeutic use; Animals; Calcium Channel Blockers; pharmacology; therapeutic use; Calcium Channels, N-Type; drug effects; Cardiomegaly; drug therapy; etiology; Dihydropyridines; pharmacology; therapeutic use; Disease Models, Animal; Male; Mice; Mice, Inbred C57BL; Nifedipine; pharmacology; therapeutic use
- From: Journal of Southern Medical University 2010;30(4):755-759
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo compare the effects of amlodipine, benidipine and nifedipine on myocardial hypertrophy and evaluate the underlying mechanism.
METHODSMyocardial hypertrophy model was created by transverse aortic constriction (TAC) in C57 BL/6 mice, and plasma catecholamine concentrations were measured 7 days after surgery to confirm the sympathetic activation. The 3 drugs were administered in TAC mice for 7 days and cardiac hypertrophy was evaluated according to the heart-to-body weight ratio (HW/BW). Effects of those drugs on the protein synthesis stimulated by phenylephrine in cultured neonatal cardiac myocytes were also examined.
RESULTSHW/BW and plasma concentrations of catecholamine were significantly increased in TAC mice one week after surgery in comparison with to sham-operated mice. One week after TAC, the HW/BW ratio was significantly lower in the amolodipine but not nifedipine-treated group than in the TAC group. Administration of nifedipine via minipump infusion for one week did not decrease HW/BW ratio. Treatment with amlodpine or benidipine, but not nifedipine, decreased the neonatal rat myocyte protein synthesis induced by phenylephrine stimulation.
CONCLUSIONAntihypertrophic effect of DHEs on myocardium is dependent on their potential of blocking N-type calcium channel, and the underlying mechanism involves the sympathetic inhibition.