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睾酮对大鼠肾髓质血管加压素受体浓度及抗利尿反应的影响。

Effects of testosterone on the rat renal medullary vasopressin receptor concentration and the antidiuretic response.

作者信息

Pávó I, Varga C, Szücs M, László F, Szécsi M, Gardi J, László F A

机构信息

Endocrine Unit, Albert Szent-Györgyi Medical University, Korányi, Hungary.

出版信息

Life Sci. 1995;56(14):1215-22. doi: 10.1016/0024-3205(95)00061-a.

Abstract

The renal concentrating ability declines with age in humans and animals. Studies suggest that the concentrating defect is due to a decrease in renal vasopressin sensitivity. With ageing, expression of the renal vasopressin V2 receptor in rat is impaired; the normal receptor expression is restored by testosterone treatment. The effect of testosterone on the renal sensitivity to vasopressin was investigated in young rats. Male rats after orchidectomy and chronic antiandrogen cyproterone acetate treatment, and female rats after chronic testosterone phenylpropionate treatment, were used. The plasma arginine-vasopressin (AVP) and testosterone concentrations, and the antidiuretic responses to AVP and the V2 agonist deamino-[8-D-arginine]-vasopressin (dDAVP) after volume loading were measured, and the renal [3H]AVP binding density was determined. The plasma AVP level decreased slightly, but not significantly, in male rats after orchidectomy and cyproterone acetate treatment, but did not alter in female rats after testosterone treatment. The AVP and dDAVP sensitivities decreased in male rats after orchidectomy and cyproterone acetate administration, and increased in female rats treated with testosterone, as compared with the animals with a normal gonadal function. [3H]AVP binding to the renal inner medullary membranes was decreased following orchidectomy or antiandrogen treatment in male rats, and increased in testosterone-treated female rats. The results suggest that testosterone may play a physiological role in maintenance of the V2 vasopressin receptor expression and hence in the normal urinary concentrating ability in rat.

摘要

在人类和动物中,肾脏的浓缩能力会随着年龄的增长而下降。研究表明,这种浓缩缺陷是由于肾脏对血管加压素的敏感性降低所致。随着年龄的增长,大鼠肾脏血管加压素V2受体的表达受损;通过睾酮治疗可恢复正常的受体表达。本研究在年轻大鼠中探讨了睾酮对肾脏血管加压素敏感性的影响。实验使用了去势并接受慢性抗雄激素醋酸环丙孕酮治疗的雄性大鼠,以及接受慢性丙酸睾酮治疗的雌性大鼠。测量了血浆精氨酸血管加压素(AVP)和睾酮浓度、容量负荷后对AVP和V2激动剂去氨基-[8-D-精氨酸]-血管加压素(dDAVP)的抗利尿反应,并测定了肾脏[3H]AVP结合密度。去势并接受醋酸环丙孕酮治疗的雄性大鼠血浆AVP水平略有下降,但无显著差异,而接受睾酮治疗的雌性大鼠血浆AVP水平未发生改变。与性腺功能正常的动物相比,去势并给予醋酸环丙孕酮的雄性大鼠对AVP和dDAVP的敏感性降低,而接受睾酮治疗的雌性大鼠的敏感性增加。去势或抗雄激素治疗后,雄性大鼠肾脏内髓质膜上的[3H]AVP结合减少,而接受睾酮治疗的雌性大鼠则增加。结果表明,睾酮可能在维持V2血管加压素受体表达以及大鼠正常的尿液浓缩能力方面发挥生理作用。

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