Wang P, Liu J, Xu S, Luo D, Sun B
Department of Pathophysiology, Third Military Medical College, Chongqing.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 1997 Feb;13(1):25-8.
The alterations of paracrine function of pulmonary arterial endothelial cells (PAEC) might play an important role in the development of hypoxic artery hypertension (HPAH). To test this hypothesis, the effects of hypoxia on angiotensin II (AT II) secretion by new born bovine PAEC were investigated. AT II secretion increased significantly when PAECs were incubated under 2.5% O2 hypoxic condition for 1.5 h (P < 0.01 vs control). But it decreased from 1.5 h to 12 h incubation and increased from 12 h to 48 h incubation under 0% O2 hypoxic condition, with significance compared with control group (P < 0.01). NO donor SIN-1 inhibited but endogenous NO inhibitor L-nitro-arginine promoted AT II secretion significantly under both normorxic and hypoxic conditions. It was also found that the concentration of cyclic guanine monophosphate in PAEC decreased significantly at 24 h incubation in 0% O2. The above results suggest that changes of AT II in PAEC may participate in the development of HPAH.
肺动脉内皮细胞(PAEC)旁分泌功能的改变可能在低氧性肺动脉高压(HPAH)的发生发展中起重要作用。为验证这一假设,研究了低氧对新生牛PAEC血管紧张素II(AT II)分泌的影响。当PAEC在2.5% O₂低氧条件下孵育1.5小时时,AT II分泌显著增加(与对照组相比,P < 0.01)。但在0% O₂低氧条件下,孵育1.5小时至12小时时分泌减少,孵育12小时至48小时时分泌增加,与对照组相比有显著性差异(P < 0.01)。在常氧和低氧条件下,NO供体SIN - 1均显著抑制AT II分泌,而内源性NO抑制剂L - 硝基精氨酸则显著促进其分泌。还发现,在0% O₂条件下孵育24小时时,PAEC中环状鸟苷单磷酸的浓度显著降低。上述结果表明,PAEC中AT II的变化可能参与了HPAH的发生发展。