The angiotensin II-aldosterone system is upregulated in a dose- and time-dependent manner following radiation-induced lung injury in a rat model, suggesting a pathophysiological role.
Hypothesis-generating for RAAS blockade in radiation lung injury; human studies needed before clinical consideration.
OBJECTIVE: Radiation-induced lung injury (RILI) is the most common, dose-limiting complication in thoracic malignancy radiotherapy. Considering its negative impact on patients and restrictions to efficacy, the mechanism of RILI was studied. METHODS: Wistar rats were locally irradiated with a single dose of 0, 16, and 20 Gy to the right half of the lung to establish a lung injury model. Two and six months after irradiation, the right half of the rat lung tissue was removed, and the concentrations of TGF-β1, angiotensin II, and aldosterone were determined via enzyme-linked immunosorbent assay. RESULTS: Statistical differences were observed in the expression levels of angiotensin II and aldosterone between the non-irradiation and irradiation groups. Moreover, the expression level of the angiotensin II-aldosterone system increased with increasing doses, and the difference was still observed as time progressed. CONCLUSIONS: Angiotensin II-aldosterone system has an important pathophysiological function in the progression of RILI.
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Cao et al. (2012) studied this question.
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