Heterogeneity of angiotensin II in endothelial nitric oxide synthase gene expression in porcine arterial endothelial cells

Objective To investigate the difference of pathophysiology between systemic and pulmonary circulation by studying the effect of angiotensin Ⅱ (AT-Ⅱ) on endothelial nitric oxide synthase (eNOS) gene expression in porcine aortic and pulmonary artery endothelial cells. Methods eNOS mRNA expression was measured by reverse transcription polymerase chain reaction (RT-PCR) and protein level by immunocytochemistry methods (LSAB). Results 6, 12, 24, 36, and 48 hours after being treated by 10-6 mol/L of AT-Ⅱ, the eNOS mRNA expression and protein level in aortic endothelial cells were decreased in a time-dependent manner and they reached to the lowest point at 24 h, being as (53.2 ± 8.1)% (P 0.01) and (45.5 ± 7.4)% (P 0.01) as those in the control group. The eNOS mRNA expression and protein level in pulmonary artery endothelial cells were downregulated in the early stage (≤24 h), being (50.6 ± 4.6)%(P 0.01) and (63.7 ± 6.5)%(P 0.01), respectively. At 48 h the eNOS mRNA expression level became normal and was as (96.5 ± 5.3)% as that in the controls (P 0.05) while the protein level was (121.7 ± 9.6)% (P 0.05). Conclusion The eNOS mRNA expression in aortic endothelial cells and that in pulmonary artery endothelial cells are affected differently by AT-Ⅱ, which may be involved in the regulation of different subtypes of AT receptors subtypes or different messenger pathways and may suggest that pathophysiological heterogeneity exists between the arteries of systemic circulation and those of pulmonary circulation.