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雌激素处理大鼠中血管紧张素诱导的饮水减少。

Attenuation of angiotensin-induced water intake in estrogen-treated rats.

作者信息

Fregly M J, Thrasher T N

出版信息

Pharmacol Biochem Behav. 1978 Oct;9(4):509-14. doi: 10.1016/0091-3057(78)90050-3.

Abstract

Chronic treatment with either estradiol benzoate (31 and 57 microgram/kg/day) or ethynyl estradiol (30 and 72 microgram/kg/day) attenuated the drinking responses of female rats to acute administration of either isoproterenol (25 microgram/kg, SC) or synthetic angiotensin II (100 and 200 microgram/kg, IP). While these studies do not rule out the possibility that attenuation of isoproterenol-induced drink in estrogen-treated rats may be associated with a defect in renin release, attention is also apparently associated with a reduced responsiveness to angiotensin II. This may be related to reduced permeability of angiotensin II at the level of the circumventricular organs of the brain; to hyporesponsiveness of receptors for angiotensin II mediating thirst in the central nervous system, or to mechanism beyond the receptor that are responsible for the conscious behavioral changes which normally accompany angiotensin II-induced thirst.

摘要

用苯甲酸雌二醇(31和57微克/千克/天)或乙炔雌二醇(30和72微克/千克/天)进行长期治疗,可减弱雌性大鼠对急性给予异丙肾上腺素(25微克/千克,皮下注射)或合成血管紧张素II(100和200微克/千克,腹腔注射)的饮水反应。虽然这些研究并未排除雌激素处理的大鼠中异丙肾上腺素诱导饮水减弱可能与肾素释放缺陷有关的可能性,但这种减弱显然也与对血管紧张素II的反应性降低有关。这可能与血管紧张素II在脑室内器官水平的通透性降低有关;与中枢神经系统中介导口渴的血管紧张素II受体反应性降低有关,或者与受体之外的机制有关,这些机制负责通常伴随血管紧张素II诱导口渴的有意识行为变化。

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