Clinical and Scientific Significance of Perimenopausal Changes in Pituitary and Ovarian Hormone Secretion

2000 ◽  
pp. 45-53 ◽  
Author(s):  
Gerson Weiss
2018 ◽  
Vol 50 (5S) ◽  
pp. 350
Author(s):  
Akemi Sawai ◽  
Risa Mitsuhashi ◽  
Yuki Warashina ◽  
Alexander Zaboronok ◽  
Ryota Sone ◽  
...  

1982 ◽  
Vol 101 (2) ◽  
pp. 268-272 ◽  
Author(s):  
Béla Zsolnai ◽  
Bertalan Varga ◽  
Edit Horváth

Abstract. Oestrous rats were anaesthetized with pentobarbital and one of the femoral arteries, femoral veins and utero-ovarian veins were cannulated. Five min blood fractions were collected from the ovary for 50 min. Following two control fractions fenoterol, noradrenaline, isoproterenol (0.5 μg/min) or 0.9% NaCl (0.02 ml/min) were infused iv for 40 min. In a group of oestrous animals fenoterol was given locally to the ovarian bursa. Blood pressure and the ovarian venous outflow were continuously recorded and blood levels of progesterone (P) and oestradiol-17β (E2) were determined by RIA. Fenoterol administered iv increased P secretion without altering ovarian blood flow, whereas noradrenaline and isoproterenol had no effect on P secretion. Fenoterol administered locally stimulated both P and E2 secretion, and this was prevented by iv infusion of propranolol. It is suggested that ovarian β2-adrenergic receptors have a regulatory role in ovarian hormone secretion.


1994 ◽  
Vol 143 (1) ◽  
pp. 13-24 ◽  
Author(s):  
B K Campbell ◽  
B M Gordon ◽  
R J Scaramuzzi

Abstract Transforming growth factor α (TGFα) inhibits hormone production by cultured follicular cells but evidence of an effect of TGFα on ovarian hormone secretion in vivo is still required. Eleven ewes with an autotransplanted ovary received, by ovarian arterial infusion, either 5 μg/h recombinant rat TGFα (n=6) or placebo (n=5) for 12 h on day 10 of the luteal phase. Two hours before the start and 1 hour before the end of the infusion each ewe received a single injection of gonadotrophin-releasing hormone (GnRH; 150 ng i.v.). Two hours after the end of the infusion luteal regression was induced with prostaglandin F2α (PGF2α; 125 μg i.m.). Ovarian and jugular venous blood samples were taken at 10-min, 15-min or 4-h intervals from 2 h before the start of the infusion until 96 h after PGF2α and the rates of secretion of ovarian oestradiol, inhibin, progesterone and androstenedione were determined. Jugular venous concentrations of LH and FSH were also measured and follicle populations monitored by real-time ultrasound scanning. Infusion of TGFα resulted in a significant (P<0.05) depression in the amplitude of the pulsatile response of oestradiol and androstenedione secretion to the GnRH-induced LH pulse at the end of the infusion. Ovarian inhibin secretion was acutely suppressed by TGFα infusion (P<0·001) and remained lower than controls for the period of the experiment. Luteal phase progesterone secretion was also acutely inhibited (P<0·001) by infusion of TGFα and in one treated ewe progesterone secretion was elevated 48–84 h after PGF2α. Jugular venous concentrations of FSH in TGFα-treated ewes were significantly (P<0·001) elevated over controls during the first 48 h of the follicular phase and the LH surge was delayed for about 10 h (P<0·05). Infusion of TGFα caused a marked decline (P<0·05) in the number of large follicles within 12 h of the end of the infusion. Two of the six treated ewes, including the one with high follicular phase progesterone, had unusually large (8·7 and 10 mm) follicles present from 48–96 h after PGF2α. We conclude that direct arterial infusion of TGFα results in acute inhibition of ovarian steroid and inhibin secretion that is associated with induction of atresia in the population of large follicles. The lack of feedback of ovarian hormones results in a rebound increase of FSH which stimulates the growth of more ovarian follicles and the eventual re-establishment of ovarian hormone secretion and normal cyclicity. Journal of Endocrinology (1994) 143, 13–24


1997 ◽  
Vol 73 ◽  
pp. 103
Author(s):  
Minoru Hatsula ◽  
Kazuhiro Tamura ◽  
Gen Watanabe ◽  
Kazuyoshi Taya ◽  
Hiroshi Kogo Kogo

1989 ◽  
Vol 3 (4) ◽  
pp. 241-247 ◽  
Author(s):  
Katalin Paksy ◽  
Bertalan Varga ◽  
Edit Horváth ◽  
Erzsébet Tátrai ◽  
György Ungváry

2018 ◽  
Author(s):  
C. Allison Stewart ◽  
M. David Stewart ◽  
Ying Wang ◽  
Rui Liang ◽  
Yu Liu ◽  
...  

AbstractFemale mice homozygous for an engineered Gnrhr E90K mutation have reduced gonadotropin-releasing hormone signaling, leading to infertility. Their ovaries have numerous antral follicles but no corpora lutea, indicating a block to ovulation. These mutants have high levels of circulating estradiol and low progesterone, indicating a state of persistent estrus. This mouse model provided a unique opportunity to examine the lack of cyclic levels of ovarian hormones on uterine gland biology. Although uterine gland development appeared similar to controls during prepubertal development, it was compromised during adolescence in the mutants. By 20 weeks of age, uterine gland development was comparable to controls, but pathologies, including squamous neoplasia, tubal neoplasia, and cribriform glandular structures, were observed. Induction of ovulations by periodic human chorionic gonadotropin treatment did not rescue post-pubertal uterine gland development. Interestingly, progesterone receptor knockout mice, which lack progesterone signaling, also have defects in post-pubertal uterine gland development. However, progesterone treatment did not rescue post-pubertal uterine gland development. These studies indicate that chronically elevated levels of estradiol with low progesterone and therefore an absence of cyclic ovarian hormone secretion disrupts post-pubertal uterine gland development and homeostasis.


Life Sciences ◽  
2021 ◽  
Vol 265 ◽  
pp. 118792
Author(s):  
Leticia Morales-Ledesma ◽  
Angélica Trujillo Hernández ◽  
María Isabel Ramírez ◽  
Gabriela Rosas ◽  
Rosa Linares

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