[Changes of angiotensin II and its receptor during the development of chronic intermittent hypoxia-induced hypertension in rats].

OBJECTIVE: To observe the changes of angiotensin II (ATII) and ATII type-1 receptor (AT1R) during the development of chronic intermittent hypoxia (CIHO)-induced hypertension in rats, and the effect in the mechanism of CIHO-induced hypertension.
METHODS: Seventy-two male Wistar rats were divided into three groups:intermittent hypoxia group (IH), sham control group (SC) and control group (UC). By using supply of nitrogen (30 s each cycle) followed by compressed air (30 s each cycle) into the exposure chambers (4% - 6% nadir ambient oxygen with return to 21%), IH rats were subjected to intermittent hypoxia every 60 s for 8 h/d during the diurnal sleep period. SC rats were similarly treated but received compressed air instead of nitrogen. UC rats were not treated. Mean arterial pressure (MAP), the levels of ATII and renin activity (RA) in plasma as well as the expression of AT1R mRNA in tissue were measured on day 7, 21 and 42 after experiment.
RESULTS: MAP was significantly elevated in IH rats [(102.2 +/- 6.2) mm Hg, 1 mm Hg = 0.133 kPa] compared with initial MAP [(94.1 +/- 4.3) mm Hg, P < 0.01] and compared with that in SC [(95.7 +/- 3.6) mm Hg], UC [(97.2 +/- 3.6) mm Hg, all P < 0.05] on day 42. The levels of ATII and RA in plasma in IH rats increased gradually over time, and RA started to increase significantly on day 7 [(3.86 +/- 1.25) ng.ml(-1).h(-1)] compared with that in SC [(2.73 +/- 0.98) ng.ml(-1).h(-1)], UC [(2.55 +/- 0.87) ng.ml(-1).h(-1), all P < 0.05], and ATII started to increase significantly on day 21 [(214 +/- 41) ng/L] compared with that in SC [(124 +/- 21) ng/L], UC [(121 +/- 18) ng/L, all P < 0.01]. The RA and ATII levels in plasma showed positive correlation with MAP (r = 0.529, P = 0.008; r = 0.475, P = 0.019 respectively). The expression of AT1R mRNA in heart, kidney and aorta in IH rats showed no differences compared with that in SC and UC group (all P > 0.05). All indices were not different between SC and UC rats at any time point (all P > 0.05).
CONCLUSION: CIHO can cause the levels of circulating RA and ATII to increase, but has no effects on AT1R mRNA expression in tissue, which suggests that activated renin-angiotensin system may contribute to the pathogenesis of CIHO-induced hypertension.