Protective Effect and Mechanism of Alprostadil in Acute Respiratory Distress Syndrome Induced by Oleic Acid in Rats

Yan, Xiujuan; Li, Yingxiu; Choi, Yun Ho; Wang, Chongyang; Piao, Yihua; Ye, Jing; Jiang, Jingzhi; Li, Liangchang; Xu, Huixian; Cui, Qingsong; Yan, Guanghai; Jin, Minggen

The renin-angiotensin system (RAS) plays a key role in maintaining blood pressure homeostasis, as well as fluid and salt balance [16] . For many years, angiotensin-converting enzyme (ACE) has been known as the key enzyme in the regulation of RAS [17] . The pulmonary circulation is an important target for the renin-angiotensin system in the lungs. ACE activity triggers vasoconstriction by generating angiotensin II from angiotensin [18] . Previous reports indicate that the RAS plays a critical role in ARDS [19] . For instance, angiotensin II (Ang II) and AT1 receptor (AT1R) induces pulmonary vasoconstriction, suggesting vital roles of Ang II and AT1R in elevating pulmonary vascular tone and causing pulmonary edema [20] . In addition, accumulating data suggest that Ang II also increases vascular permeability via AT1R [21] . Several mediators have been implicated in Ang II-regulated vascular permeability changes, including the eicosanoids leukotriene C4, prostaglandin E2 and prostaglandin I2, and vascular permeability factor [22] . Therefore, ACE functions as a lung-injury-promoting factor in ALI, which needs to be controlled during the treatment and prevention of ARDS.