Testosterone maintains pituitary and serum FSH and spermatogenesis in gonadotrophin-releasing hormone antagonist-suppressed rats.

Testosterone maintains pituitary and serum FSH and spermatogenesis in gonadotrophin-releasing hormone antagonist-suppressed rats.
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睾酮维持促性腺激素释放激素拮抗剂抑制大鼠的垂体和血清 FSH 以及精子发生。

DOI:
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发表时间:
1986
影响因子:
4
通讯作者:
E. Nieschlag
E. Nieschlag
中科院分区:
医学2区
文献类型:
--
作者:
M. Rea;G. Marshall;G. Weinbauer;E. Nieschlag

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成年雄性大鼠组连续接受溶媒或强效促性腺激素释放激素(GnRH)拮抗剂治疗30天。(N-Ac-D-Nal(2)1、D-pCl-Phe2、D-Trp3、D-hArg(Et2)6、D-Ala10)- GnRH(RS 68439; 35 μ g/天)。此外,媒介物和拮抗剂处理的大鼠组接受s.c.睾酮植入物足以维持血清睾酮浓度比赋形剂处理的对照大鼠高3.5- 5倍。拮抗剂处理30天后,血清LH、FSH和睾酮浓度等于或低于其各自试验的检测限,垂体FSH含量和GnRH受体结合率相对于对照动物分别降低77%和98%。在拮抗剂治疗的大鼠睾丸重量减少了75%,精子发生被抑制的程度与垂体切除大鼠中观察到的。与对照组动物相比,替吉奥导致血清FSH降低40%,可阻止拮抗剂诱导的血清和垂体FSH下降,但不能阻止GnRH受体下降,低于溶媒加睾酮给药组中观察到的水平。此外,拮抗剂加睾酮处理组的精子发生与对照动物中观察到的精子发生无区别。它的结论是,睾酮是能够维持血清和垂体FSH水平在体内,条件下,这可能使垂体不敏感下丘脑GnRH。
Groups of adult male rats were treated continuously for 30 days with either vehicle or the potent gonadotrophin-releasing hormone (GnRH) antagonist. (N-Ac-D-Nal(2)1,D-pCl-Phe2,D-Trp3,D-hArg(Et2)6,D-Ala10 )- GnRH (RS 68439; 35 micrograms/day). In addition, groups of vehicle- and antagonist-treated rats received s.c. testosterone implants sufficient to maintain serum testosterone concentrations 3.5- to 5-fold higher than those of vehicle-treated control rats. After 30 days of antagonist treatment serum LH, FSH and testosterone concentrations were at or below the detection limits of their respective assays and pituitary FSH content and GnRH receptor binding were reduced, relative to control animals, by 77 and 98% respectively. Testis weight in antagonist-treated rats was reduced by 75% and spermatogenesis was suppressed to an extent comparable to that observed in hypophysectomized rats. Testosterone, which caused a 40% reduction in serum FSH relative to control animals, prevented the antagonist-induced fall in both serum and pituitary FSH, but not GnRH receptors, below that observed in the vehicle plus testosterone-treated group. Furthermore, spermatogenesis in the antagonist plus testosterone-treated group was indistinguishable from that observed in control animals. It is concluded that testosterone is capable of maintaining serum and pituitary FSH levels in vivo, under conditions which presumably render the pituitary insensitive to hypothalamic GnRH.