Role of Renin-Angiotensin System, Renal Nerve System, and Oxidative Stress in Chronic Stress-Induced Renal Expression of Aquaporin-1 in Rats

Abstract

Aims: To investigate the renal aquaporin-1 (AQP1) expression under chronic stress (induced by foot shock) condition and possible mechanisms involved in rats. Methods: The chronic stress model was established in male Sprague Dawley (SD) rats by foot shock for two weeks. Rats were randomly divided into control group, chronic stress group, renal denervation group, renal denervation plus chronic stress group, captopril (an angiotensin I converting enzyme inhibitor, ACEI) plus chronic stress group and tempol (a superoxide dismutase mimetic) plus chronic stress group. Body weight, food intake, water intake, blood pressure and heart rate were monitored. Real-time PCR was used to detect the mRNA level of AQP1 in the renal tissue. Immunohistochemistry stain was used to observe the expression and location of AQP1 in rat kidneys. Results: Chronic stress reduced body weight gain and food intake, while it significantly increased systolic blood pressure and renal expressions of mRNA and protein of AQP1 (P<0.05) as compared with control group. Renal denervation and tempol treatments did not affect stress-induced decreases of body weight gain and food intake. Renal denervation, captopril and tempol treatments decreased systolic blood pressure. Compared with the chronic stress group, mRNA and protein expression of AQP1 was decreased (P<0.05) in renal denervation plus chronic stress group, captopril plus chronic stress group and tempol plus chronic stress group. Conclusion: Chronic stress induces increase of the AQP1 expression in kidney, which is regulated by renal nerve system, renin-angiotensin system and oxidative stress.