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镉诱导的大鼠高血压

Cadmium-induced hypertension in rats.

作者信息

Balaraman R, Gulati O D, Bhatt J D, Rathod S P, Hemavathi K G

机构信息

Pharmacy Department, Faculty of Technology and Engineering, Kalabhavan, M.S. University of Baroda, India.

出版信息

Pharmacology. 1989;38(4):226-34. doi: 10.1159/000138541.

Abstract

Chronic cadmium chloride (CdCl2, 0.5 and 1.0 mg/kg, i.p.) treatment in female albino rats for 2 weeks resulted in elevation of blood pressure. In chronic CdCl2-treated rats the pressor responses to different doses of noradrenaline, angiotensin II and depressor responses to acetylcholine and isoprenaline were unaltered. In rat hindquarter preparation there was elevation of perfusion pressure and the sensitivity of vascular bed to noradrenaline was increased in the CdCl2-induced hypertensive rats. Complete bilateral adrenalectomy or chemical sympathectomy or treatment with captopril did not prevent the development of CdCl2-induced hypertension. Treatment with verapamil (15 mg/kg/day, p.o.) or nifedipine (10 mg/kg/day, p.o.) for 2 weeks prevented the development of hypertension with chronic CdCl2 treatment. It is suggested that chronic treatment of rats with CdCl2 induces hypertension. It is possible that cadmium mimics the calcium ion for the induction of hypertension in rats.

摘要

对白化雌性大鼠腹腔注射氯化镉(CdCl2,0.5毫克/千克和1.0毫克/千克),连续处理2周会导致血压升高。在慢性CdCl2处理的大鼠中,对不同剂量去甲肾上腺素、血管紧张素II的升压反应以及对乙酰胆碱和异丙肾上腺素的降压反应均未改变。在大鼠后肢制备实验中,CdCl2诱导的高血压大鼠的灌注压升高,血管床对去甲肾上腺素的敏感性增加。双侧肾上腺完全切除、化学性交感神经切除术或用卡托普利治疗均不能预防CdCl2诱导的高血压的发生。用维拉帕米(15毫克/千克/天,口服)或硝苯地平(10毫克/千克/天,口服)治疗2周可预防慢性CdCl2处理导致的高血压的发生。提示用CdCl2对大鼠进行慢性处理可诱发高血压。镉有可能在诱导大鼠高血压方面模拟了钙离子的作用。

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