The functional changes in L-type Ca2+ channel of hypertrophied cardiomyocytes in neonatal rats induced by angiotensin II.
- Author:
Qiu-Li YAN
1
;
Wei HUA
;
Liang-Zhu YU
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; adverse effects; Animals; Calcium; metabolism; Calcium Channels, L-Type; metabolism; Female; Hypertrophy; metabolism; Male; Membrane Potentials; Myocytes, Cardiac; metabolism; pathology; physiology; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2013;29(1):91-95
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the molecular and functional changes in L-type Ca2+ channel of hypertrophied cardiomyocytes in neonatal rats induced by angiotensin II (Ang II).
METHODSThe in vitro model of cardiomyocyte hypertrophy was established in cultured cardiomyocytes from neonatal rats. Whole cell patch clamp was used to measure the L-type Ca2+ currents. Semi-quantitative RT-PCR was used to determine the mRNA expression of L-type Ca2+ channel alpha1C subunits.
RESULTSIn the hypertrophied cardiomyocytes induced by Ang II, I(Ca, L) densities were increased, whereas the features of I(Ca,L) activation, inactivation or recovery from inactivation were not affected. Meanwhile, Ang II increased the mRNA expression of L-type Ca2+ channel alpha1C subunits in cardiomyocytes. All these actions of Ang II could be blocked by the angiotensin II 1 type receptor blocker losartan.
CONCLUSIONDuring cardiomyocyte hypertrophy induced by Ang II, there are significant changes in the molecule and function of L-type Ca2+ channels, which are mediated by the angiotensin II 1 type receptor.
