Valiquette G, Martini L
Acta Endocrinol (Copenh). 1982 Apr;99(4):493-9. doi: 10.1530/acta.0.0990493.
The secretion of vasopressin has been shown recently to be influenced by gonadal steroids. To further evaluate the relevance of sex steroids in the control of vasopressin secretion, the vasopressin response to dehydration has been studied in normal, castrated and sex-steroid treated castrated male rats. Short-term (3 weeks) castration did not modify the vasopressin response to 48 h of water deprivation. Long-term (10 weeks) castration, on the other hand, consistently reduced the vasopressin response by more than 50%. In both cases, the osmolality was unaffected. Treatment of long-term castrated rats with testosterone, dihydrotestosterone, or oestradiol increased the vasopressin response to dehydration towards normal control levels. However, only oestradiol could restore it to and beyond normal levels, although all three steroids were given in doses that were equipotent in bringing back to normal the plasma LH levels of the castrated animals. Angiotensin-II generation may indirectly be augmented by oestradiol treatment and this may account for the effect of oestradiol here reported. No such mechanism, however, may be invoked in the case of androgens; a direct modulatory effect at the hypothalamic level is postulated for explaining their influence on vasopressin secretion.
最近研究表明，血管加压素的分泌受性腺类固醇影响。为了进一步评估性类固醇在血管加压素分泌调控中的相关性，我们对正常、去势及经性类固醇处理的去势雄性大鼠进行脱水处理，研究血管加压素的反应。短期（3周）去势并未改变血管加压素对48小时禁水的反应。另一方面，长期（10周）去势则持续使血管加压素反应降低超过50%。两种情况下，渗透压均未受影响。用睾酮、双氢睾酮或雌二醇治疗长期去势大鼠，可使血管加压素对脱水的反应增加至正常对照水平。然而，尽管给予三种类固醇的剂量在使去势动物血浆促黄体生成素水平恢复正常方面等效，但只有雌二醇能将其恢复至正常水平以上。雌二醇治疗可能间接增加血管紧张素II的生成，这可能解释了此处报道的雌二醇的作用。然而，雄激素的情况可能不存在这种机制；推测其对血管加压素分泌的影响是通过下丘脑水平的直接调节作用实现的。
