Figure 1.
Effects of Ach on relaxation of rings in E+ and E− of normoxic and CIH rats pulmonary arteries.
Pulmonary artery rings were pre-contracted with PE (10−6 M), and relaxation to ACh was detected. Relaxant responses to ACh were expressed as a percentage of PE-induced tone. Data were means ± SD; n = 6. **P<0.01, *P<0.05, relative to normoxia, E+.
Figure 2.
Effects of ET-1 on endothelium-intact (E+) and endothelium-denuded (E−) pulmonary arteries from normoxia and CIH rats.
Contraction was expressed as an isometric tension (A) and a normalized isometric tension. The Emax was 0.42±0.02 nmol/L for Normoxia (E+), 0.69±0.01 nmol/L for CIH (E+), 0.60±0.02 nmol/L for Normoxia (E−) and 0.73±0.02 for CIH (E−), respectively. The EC50 was 0.72±0.17 nmol/L for Normoxia (E+), 0.47±0.08 nmol/L for CIH (E+), 0.30±0.03 nmol/L for Normoxia (E−) and 0.21±0.04 for CIH (E−), respectively. **P<0.01.
Figure 3.
Effects of BQ-123 and BQ-788 on contraction of rat pulmonary arteries to ET-1.
Results were expressed as an isometric tension (A and B) and the percentage of the difference to pre-contraction (C). Data were means ± SD; n = 6. ##P<0.01, compared with pre-contraction with ET-1., **P<0.01.
Figure 4.
Effects of L-NAME on contraction of rats pulmonary arteries to ET-1.
Results were expressed as an isometric tension (A) and the percentage of the difference to pre-contraction (B). Data were means ± SD; n = 6. ##P<0.01, compared with pre-contraction with ET-1., **P<0.01.
Figure 5.
Effects of CIH on pulmonary arteries histopathological changes.
Representative microscopic photographs of pulmonary arteries stained with H&E (magnification 400×) (A and B) and TEM (C and D). Pulmonary arteries obtained from normoxia group (A and C) and CIH group (B and D). In the pulmonary artery segments from the CIH group, there were histopathological changes of the endothelial monolayer with cellular enlargement and edema, denudation of some endothelial cells. The ultrastructure was observed by TEM in the (C) normoxia group and (D) CIH group. Large defects of the endothelial layer, cellular vacuolation and mitochondrial damage could be observed in D.
Figure 6.
Effects of CIH on ET-1, ETA receptor and ETB receptor localization in pulmonary arteries were analyzed by immunohistochemistry.
Immunoreactivity for ET-1 and ETA receptor increased in the media and intima of the pulmonary artery after exposure to CIH. Meanwhile, immunoreactivity for the ETB receptor decreased markedly in the intima and there was no significant change in the media of the pulmonary artery after exposure to CIH.
Figure 7.
Effects of CIH on ET-1, ETA receptor and ETB receptor expression in pulmonary arteries.
Equal loading of protein was confirmed using an anti-GAPDH antibody. Quantification of the protein expression was normalized to GAPDH. **P<0.01.
Figure 8.
Effects of CIH on eNOS expression and NO level in pulmonary arteries.
Effects of CIH on eNOS expression in pulmonary arteries were analyzed by western blot (A). Equal loading of protein was confirmed using an anti-GAPDH antibody. Quantification of the eNOS expression was normalized to GAPDH. The level of NO in the pulmonary artery (B) in CIH rats was dramatically reduced, compared with the normoxia group. Results are presented as means ± SD (n = 6). **P<0.01, compared with normoxia group.