[The changes of angiotensin II receptor expression in cardiomyocytes of ventricles in pigs with experimental ventricular septal defect].
OBJECTIVE
To investigate the changes of angiotensin II receptors expression in cardiomyocytes of both ventricles in pigs with experimental ventricular septal defect (VSD).


METHODS
Nineteen young pigs were divided into 3 groups: the pigs that received operation to produce experimental VSD, the pigs that underwent sham-operation, and the pigs as normal control. One month after the operation, the pigs were catheterized and then put to death; the cardiomyocytes were taken from their ventricles and were isolated. Radioligand binding assay was done to measure the Bmax and KD of angiotensin II receptor per 10(6) cells.


RESULTS
For both Bmax and KD of angiotensin II receptors, there were no significant differences between the sham-operation group and the control. The Bmax of left ventricle AT1R (188.42 +/- 133.97 fmol/10(6)) and Bmax of right ventricle AT1R (272.14 +/- 232.74 fmol/10(6)) and AT2R (40.42 +/- 34.76 fmol/10(6)) in the operation group were significantly elevated in comparison with the control (Bmax of left ventricle AT1R 29.20 +/- 19.50 fmol/L, and Bmax of right ventricle AT1R 76.72 +/- 51.21 fmol/L and AT2R 9.63 +/- 1.27 fmol/L) respectively, P < 0.05.


CONCLUSIONS
Intracardiac left-to-right shunt related volume overload leads to the elevation of AT1R expression in cardiomyocytes, which serves as an important mechanism of ventriclular hypertrophy and remodling in congenital heart disease. The increased expression of AT2R in right ventricle is a possible explanation of the phenomenon that moderately sized VSDs usually show left other than right ventriclular hypertrophy, taking into account that AT2R has been suggested to mediate antitrophic reaction.
Zhou
Tongfu
T
Department of Pediatric Cardiology, Second West China Hospital, Sichuan University, Chengdu 610041, China.
Dong
Liqun
L
Zhang
Min
M
Li
Mi
M
Hua
Yimin
Y
Liu
Hanmin
H
Tao
Dachang
D
Li
Qiang
Q
D000818:Animals; D005260:Female; D006345:Heart Septal Defects, Ventricular / Q000150:complications / Q000378:metabolism*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology / Q000378:metabolism; D008297:Male; D032383:Myocytes, Cardiac / Q000378:metabolism*; D011945:Receptors, Angiotensin / Q000378:metabolism*; D013552:Swine
D011945:Receptors, Angiotensin