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目的观察慢性间歇低氧诱发大鼠高血压发病过程中内皮素(ET)及其受体的动态变化,探讨慢性间歇低氧诱发高血压的发病机制。方法将Wistar大鼠(n=72)随机均分为间歇低氧组(IH组)、实验对照组(SC组)和空白对照组(UC组)。IH组大鼠循环给予氮气和压缩空气(每一循环60s,使舱内最低氧浓度达4%~6%,然后恢复至21%,8h/d),SC组大鼠循环给予压缩空气,UC组大鼠不给予任何处理。观察第7、21、42天时各组大鼠的血压、血浆ET-1水平及不同组织ET-1和内皮素A型受体(ETAR)mRNA的表达。结果第42天时IH组大鼠平均动脉压(MAP)较实验前升高约8mmHg(P<0·01),而两对照组大鼠MAP无显著变化。IH组大鼠血浆ET-1水平随间歇低氧时间的延长逐渐升高,从第7天[(157±35)ng/L]开始显著高于SC组[(123±29)ng/L]和UC组[(119±28)ng/L]水平(P<0·05),并且与MAP呈正相关(r=0·605,P=0·002);其心脏和肾皮质ET-1mRNA的表达随间歇低氧时间的延长也逐渐增加,从第21天开始显著高于两对照组水平(P<0·05);其主动脉、心脏和肾皮质ETARmRNA的表达与两对照组比较,差异无显著性(P>0·05)。SC组与UC组比较,各项观察指标差异均无显著性(P>0·05)。结论慢性间歇低氧可导致ET-1表达增加,使血循环ET-1水平升高,而对ETAR的表达没有影响,提示ET-1的过度表达可能是慢性间歇低氧诱发高血压的重要原因之一。
Objective To observe the dynamic changes of endothelin (ET) and its receptors during chronic intermittent hypoxia-induced hypertension in rats and to explore the pathogenesis of chronic intermittent hypoxia-induced hypertension. Methods Wistar rats (n = 72) were randomly divided into intermittent hypoxia group (IH group), experimental control group (SC group) and blank control group (UC group). The IH group rats were given nitrogen and compressed air (60s per cycle, the lowest oxygen concentration in the cabin was 4% ~ 6%, then recovered to 21%, 8h / d) Rats were not given any treatment. The blood pressure, plasma ET-1 level and the expression of ET-1 and ETAR mRNA in different tissues were observed on the 7th, 21st and 42nd days. Results On day 42, mean arterial pressure (MAP) of rats in IH group was increased by about 8 mmHg (P <0.01) compared with that of the control group, while no significant changes were found in MAP of the two control groups. The level of plasma ET-1 in IH group increased gradually with the prolongation of intermittent hypoxia, and was significantly higher than that in SC group [(123 ± 29) ng / L] on day 7 [(157 ± 35) ng / L] (119 ± 28) ng / L] in UC group (P <0.05), and positively correlated with MAP (r = 0.605, P = 0.002). The levels of ET-1 mRNA in heart and renal cortex The expression of ETAR mRNA also increased gradually with intermittent hypoxia and began to increase significantly from day 21 onwards (P <0.05). The expression of ETAR mRNA in the aorta, heart and renal cortex was significantly lower than that of the two control groups No significant (P> 0.05). There was no significant difference between SC group and UC group (P> 0.05). Conclusions Chronic intermittent hypoxia can lead to the increase of ET-1 expression and the increase of circulating ET-1 level, but has no effect on the expression of ETAR, suggesting that ET-1 overexpression may be an important cause of chronic intermittent hypoxia-induced hypertension one.