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目的观察应激性高血压大鼠血浆中醛固酮水平的变化,并从肾上腺微观结构方面探讨其病理基础。方法将SPF级雄性Wistar大鼠30只,随机分为正常组(10只)和应激性高血压大鼠模型组(20只)。间断足底电刺激结合噪音及制动夹尾刺激构建慢性应激性高血压大鼠模型,采用特异性放射免疫测定大鼠血浆中醛固酮的变化,通过电镜观察肾上腺皮质超微结构的变化。结果 (1)与正常组比较,模型组大鼠收缩压和舒张压均明显升高(P<0.05);(2)与正常组相比,模型组大鼠血浆中醛固酮的含量明显增高,差异有统计学意义(P<0.05);(3)正常组大鼠肾上腺皮质细胞的胞核界限清晰,而应激性高血压模型组大鼠中细胞核不规则且固缩。结论(1)本研究成功建立应激性高血压大鼠模型;(2)应激刺激作用下醛固酮含量的升高可能是造成慢性应激大鼠血压升高的重要因素;(3)高的醛固酮(ALD)水平伴随高血压共同对肾脏产生了一定的损害。
Objective To observe the change of plasma aldosterone level in stress-induced hypertension rats and to explore its pathological basis from the adrenal microstructure. Methods Thirty SPF male Wistar rats were randomly divided into normal group (n = 10) and stress-induced hypertensive rat model group (n = 20). The rat model of chronic stress-induced hypertension was established by intermittent electrical stimulation combined with noise and tail-brake stimulation. The changes of aldosterone in plasma were detected by specific radioimmunoassay. The ultrastructure of adrenal cortex was observed by electron microscopy. Results (1) Compared with the normal group, the systolic and diastolic pressure of the model group were significantly increased (P <0.05); (2) Compared with the normal group, the content of aldosterone in the model group was significantly increased (P <0.05). (3) The nuclei of adrenocortical cells in normal rats were clear, but the nuclei of rats in stress-induced hypertensive rats were irregular and condensed. Conclusions (1) The model of stress-induced hypertension is successfully established in this study. (2) The increase of aldosterone content under stress stimulation may be an important factor in the increase of blood pressure in chronic stress rats. (3) Aldosterone (ALD) levels associated with hypertension together have some damage to the kidneys.