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肾上腺切除术和肾切除术对大鼠肾上腺再生性高血压的影响。

Effects of adrenalectomy and nephrectomy on adrenal regeneration hypertension in the rat.

作者信息

Chan J Y, Chan S H

机构信息

Department of Medical Research, Veterans General Hospital-Taipei, Taiwan, Republic of China.

出版信息

Proc Natl Sci Counc Repub China B. 1991 Oct;15(4):197-205.

PMID:1815260
Abstract

The involvement of the regenerating adrenal gland and kidney, and the contribution of deoxycorticosterone (DOC) and prostaglandin E2 (PGE2), in the development of adrenal regeneration hypertension (ARH) was evaluated in young female Sprague-Dawley rats. Based on tail-cuff plethysmographic measurement, animals subjected to nephrectomy and adrenalectomy on the right side and adrenal enucleation (removal of the adrenal cortex) on the left side developed significant (P less than 0.05, n = 12) hypertension within 6 weeks following operation. Subsequent left nephrectomy in these ARH rats produced a further elevation, whereas a secondary adrenalectomy resulted in an acute and discernible reduction in blood pressure within 24-36 hours. It is interesting to note that the progressive increase in blood pressure following left nephrectomy was significantly reversed by PGE2 (10 or 20 micrograms/kg, i.p.). At the same time, the reduction in blood pressure after secondary adrenalectomy was significantly retarded by deoxycorticosterone trimethylacetate (2 mg/kg, i.p.). These data demonstrated that both the kidney and the regenerating adrenal cortex are involved in the pathogenesis of ARH. Furthermore, it is probable that the secretion of DOC by the regenerating adrenal cortex is responsible for the elevation in blood pressure, in a process that is balanced by PGE2, possibly secreted by the kidney.

摘要

在年轻雌性斯普拉格 - 道利大鼠中,评估了再生肾上腺和肾脏的参与情况,以及脱氧皮质酮(DOC)和前列腺素E2(PGE2)在肾上腺再生性高血压(ARH)发展中的作用。根据尾套体积描记法测量,右侧接受肾切除术和肾上腺切除术且左侧接受肾上腺去核术(切除肾上腺皮质)的动物在术后6周内出现了显著(P<0.05,n = 12)的高血压。这些ARH大鼠随后进行左肾切除术会使血压进一步升高,而二次肾上腺切除术则会在24 - 36小时内导致血压急剧且明显下降。有趣的是,左肾切除术后血压的逐渐升高被PGE2(10或20微克/千克,腹腔注射)显著逆转。同时,二次肾上腺切除术后血压的下降被三甲基醋酸脱氧皮质酮(2毫克/千克,腹腔注射)显著延缓。这些数据表明,肾脏和再生的肾上腺皮质均参与了ARH的发病机制。此外,再生肾上腺皮质分泌的DOC可能是血压升高的原因,在此过程中由可能由肾脏分泌的PGE2进行平衡。

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