Burke-Wolin T, Wolin M S
Department of Physiology, New York Medical College, Valhalla 10595.
J Appl Physiol (1985). 1989 Jan;66(1):167-70. doi: 10.1152/jappl.1989.66.1.167.
The effects of O2 tension on force in precontracted isolated pulmonary arterial smooth muscle from calf lungs was characterized to investigate the mechanism of O2 tension sensing. These arteries display a decrease in force with increasing O2 tension that is antagonized via inhibition of soluble guanylate cyclase activation by 10 microM methylene blue or inactivation of catalase by pretreatment with 50 mM 3-amino-1,2,4-triazole for 30 min. O2 tension-dependent relaxation is associated with an increase in intracellular H2O2 metabolism through catalase (detected as the peroxide-dependent inactivation of tissue catalase activity by aminotriazole) and cyclic guanosine 5'-monophosphate (cGMP), known mediators of relaxation in calf pulmonary arteries. Thus a recently reconstructed mechanism of activation of soluble guanylate cyclase involving the metabolism of H2O2 by catalase appears to function as an O2 tension sensor in pulmonary arteries.
为研究氧分压传感机制，对来自小牛肺脏的预收缩离体肺动脉平滑肌中氧分压对张力的影响进行了表征。随着氧分压升高，这些动脉的张力降低，通过用10微摩尔亚甲蓝抑制可溶性鸟苷酸环化酶激活或用50毫摩尔3-氨基-1,2,4-三唑预处理30分钟使过氧化氢酶失活，这种降低作用会受到拮抗。氧分压依赖性舒张与通过过氧化氢酶增加细胞内过氧化氢代谢（通过氨基三唑检测为组织过氧化氢酶活性的过氧化物依赖性失活）以及环鸟苷酸（cGMP）有关，cGMP是小牛肺动脉舒张的已知介质。因此，一种最近重建的涉及过氧化氢酶对过氧化氢代谢的可溶性鸟苷酸环化酶激活机制似乎在肺动脉中充当氧分压传感器。
