[Expression and variation of angiotensin II type 1 receptor on vascular smooth muscle cells of systemic and pulmonary circulations in experimental ventricular septal defect in pigs].

OBJECTIVE

To investigate the expression of angiotensin II type 1 receptor (AT1R) on the vascular smooth muscle cells (VSMC) of both systemic and pulmonary circulations and their variation caused by intracardiac left to right shunting using an animal model of the ventricular septal defect (VSD).

METHODS

Nineteen young pigs were divided into 3 groups: operation (experimental VSD), sham-operation, and normal control. One month after operation, the pigs were catheterized and then put to death. Smooth muscle cells were taken from aorta, pulmonary artery, pulmonary arteriole, mesenteric arteriole and VSMC were isolated. Radioligand binding assay for AT1R was done to measure the Bmax and KD.

RESULTS

There were no significant differences in Bmax and KD of AT1R between the sham-operation group and the control. Bmax of the aorta (112.11+/-35.77) fmol/10(6), main pulmonary artery (52.37+/-31.09) fmol/10(6) and mesenteric arteriole (106.98+/-100.48) fmol/10(6) in the operation group were remarkably elevated in comparison with the control (P<0.05). In the operation group, Bmax of the aorta VSMC was higher than that of main pulmonary artery VSMC (P<0.05), and Bmax of the mesenteric arteriole VSMC was higher than that of the small pulmonary arteriole VSMC (P<0.05).

CONCLUSION

The findings in AT1R expression in experimental VSD were supportive to the previously proposed hypothesis that ATR expression might be stronger in systemic VSMC than in pulmonary VSMC in young animal, especially in the presence of intracardiac left to right shunt, which may provide a sound rationale for the pharmacological management of VSD infants with angiotensin converting enzyme inhibitor or AT1R antagonist.