scholarly journals Effect of steroid- and inhibin-free ovine follicular fluid on ovarian follicles and ovarian hormone secretion

Reproduction ◽  
1991 ◽  
Vol 93 (1) ◽  
pp. 81-96 ◽  
Author(s):  
B. K. Campbell ◽  
H. M. Picton ◽  
G. E. Mann ◽  
A. S. McNeilly ◽  
D. T. Baird
1996 ◽  
Vol 149 (3) ◽  
pp. 531-540 ◽  
Author(s):  
B K Campbell ◽  
R J Scaramuzzi

Abstract Recombinant human inhibin A (rhInh) or steroid-free bovine follicular fluid (bFF) were infused into the ovarian artery of anoestrous ewes with ovarian autotransplants induced to ovulate with a pulsatile regimen of GnRH applied after a 10-day pretreatment with progestagen sponges. In the period 12–24 h after sponge withdrawal ewes received ovarian arterial infusions of saline (n=6), 0·3 μg rhInh/h (n=5), 1·6 μg rhInh/h (n=5) or 25 μl bFF/h (n=4). Controls had a normal follicular phase with an LH surge 43 ± 3 h after sponge withdrawal which resulted in ovulation (six out of six). Both doses of rhlnh increased ovarian venous inhibin concentrations in a dose-related fashion (P<0·05) but resulted in depressions (P<0·05) in FSH concentrations of similar magnitude. Both doses of rhInh acutely inhibited ovarian oestradiol and androstenedione secretion (P<0·01) but at the end of rhInh infusion oestradiol secretion was quickly re-established without a corresponding increase in FSH. LH surges were detected in five out of five and three out of five ewes infused with low and high doses of rhInh respectively, and progesterone concentrations during the subsequent luteal phase were depressed (P<0·05). Infusion of bFF had no effect on inhibin or FSH concentrations but resulted in acute inhibition (P<0·01) of ovarian oestradiol, androstenedione and inhibin secretion, a delay (P<0·05) in the time to the LH surge and a depression (P<0·05) in luteal-phase progesterone concentrations. In conclusion, while the depression in FSH induced by rhlnh cannot be excluded as a cause for the inhibitory effects of rhInh treatment on ovarian function, such a mechanism cannot fully explain the ovarian responses obtained to rhInh infusion. These results therefore support a direct ovarian role for inhibin in the modulation of ovarian function in addition to its indirect role in controlling FSH. This conclusion is supported by the demonstration that bFF can induce similar inhibitory effects on ovarian function without changing FSH. Journal of Endocrinology (1996) 149, 531–540


1990 ◽  
Vol 127 (1) ◽  
pp. 23-32 ◽  
Author(s):  
D. T. Baird ◽  
B. K. Campbell ◽  
A. S. McNeilly

ABSTRACT An experiment was conducted to examine the effect of steroid-free ovine follicular fluid (oFF) on ovarian hormone secretion. Eight Merino × Finnish Landrace ewes in which the left ovary and vascular pedicle had been autotransplanted to a site in the neck were studied during the breeding season. Luteal regression was induced in all animals by injection of cloprostenol (100 μg, i.m.) on day 10 of the luteal phase. Four of the eight animals were treated with steroid-free oFF (3 ml, s.c.) in the early follicular phase, 24 and 36 h after injection of cloprostenol. Samples of both ovarian and jugular venous blood were collected at 4-h intervals from 20 h before until 96 h after injection of cloprostenol. Ovarian and jugular venous blood samples were also collected at 10-min intervals from 48 to 52 h after injection of cloprostenol to investigate the pattern of pulsatile secretion of ovarian hormones. Samples were assayed for oestradiol, androstenedione, testosterone and inhibin and the ovarian secretion rates calculated. Both injections of oFF resulted in a fourfold increase in the concentration of inhibin in jugular venous plasma within 4–8 h of administration (P < 0·01) with concentrations remaining increased (P < 0·05) until 56 h after cloprostenol (32 h after the first oFF injection). Following oFF injection there was a profound (100%; P < 0·001) and prolonged decrease in the peripheral concentration of FSH until 60 h after cloprostenol at which time the concentration of FSH increased five- to sixfold (P < 0·001) to a peak lasting 24 h. In contrast to FSH, the concentration of LH in jugular venous plasma rose immediately following oFF treatment and continued to increase, exhibiting a profile similar to that described for FSH. No preovulatory LH surge was detected in any of the oFF-treated ewes while untreated ewes had an LH surge within 58·0±1·2 (s.e.m.) h. Within 8 h of the first injection of oFF the ovarian secretion rate of oestradiol, androstenedione and inhibin began to decline to reach a nadir of less than 1 ng/min within 32–36 h (56–60 h after cloprostenol; P < 0·01). Testosterone secretion, already barely detectable, did not change significantly following injection of oFF but remained low for 36 h following oFF and did not exhibit the increase observed over this period in controls. After injection of oFF the episodic secretion of oestradiol, androstenedione, testosterone and inhibin was markedly suppressed in spite of numerous pulses of LH. Re-establishment of inhibin, androstenedione and testosterone secretion began from around 36 h after injection of oFF and continued to increase for the remainder of the experimental period (P < 0·001). The re-establishment of oestradiol secretion, however, took until 60 h after oFF treatment (84 h after cloprostenol). This increase in ovarian hormone secretion was temporally related to the decrease in the concentration of FSH and LH in jugular venous plasma that was observed at the end of the experimental period. We conclude that treatment of ewes with steroid-free oFF during the follicular phase of the oestrous cycle results in the immediate inhibition of the ovarian secretion of oestradiol, inhibin, androstenedione and testosterone. This effect can most probably be attributed to the depression in FSH that occurs following oFF injection, although the possibility exists that other factors present in oFF are acting directly on the ovary to inhibit follicular growth. Journal of Endocrinology (1990) 127, 23–32


1974 ◽  
Vol 77 (3) ◽  
pp. 575-587 ◽  
Author(s):  
F. H. de Jong ◽  
D. T. Baird ◽  
H. J. van der Molen

ABSTRACT The concentrations of oestradiol-17β, oestrone, androstenedione, testosterone, dehydroepiandrosterone, dehydroepiandrosterone sulphate and progesterone were measured in ovarian venous plasma from one or both ovaries in 4 normal women during different stages of the menstrual cycle and in 4 women with persistent ovarian follicles. In addition the steroid concentrations in peripheral plasma and follicular fluid were estimated. All steroids mentioned, with the exception of dehydroepiandrosterone sulphate, were secreted by the ovaries. The concentrations of oestradiol-17β, oestrone, androstenedione and progesterone were higher in the venous plasma from the ovary containing the developing follicle or corpus luteum than in venous plasma from the contralateral ovary. There was a good correlation between ovarian secretion of the oestrogenic steroids and androstenedione. Finally, the quantitative contribution of the ovarian secretion to the blood production rates of the androgens and progesterone was calculated. The only contributions exceeding 20 % of the blood production rate were those of progesterone and androstenedione during the second half of the cycle.


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

2020 ◽  
Vol 103 (5) ◽  
pp. 1069-1084
Author(s):  
Adam J Ziecik ◽  
Klaudia Drzewiecka ◽  
Katarzyna Gromadzka-Hliwa ◽  
Jan Klos ◽  
Patrycja Witek ◽  
...  

Abstract Altrenogest with gonadotropins is commonly used to synchronize the estrous cycle, but it can also lead to follicular cyst formation, especially in prepubertal gilts. Here, we aimed to investigate how maturity and altrenogest treatment affect the development, endocrine milieu, and molecular control of ovarian follicles. Crossbred prepubertal and mature gilts were challenged or not (control) with altrenogest, and ovaries were collected in the morning on the first day of behavioral estrus. In prepubertal gilts, altrenogest decreased the percentage of primordial and atretic small follicles, but increased large antral follicles when compared with controls. In mature gilts, altrenogest reduced the percentage of primary follicles and elevated the total number of antral follicles. Maturity affected the estradiol level in the follicular fluid of preovulatory follicles, luteinizing hormone (LH)-stimulated cyclic adenosine monophosphate (cAMP) generation, and LH receptor messenger RNA (mRNA) expression in granulosa. Moreover, cytochrome P45017A1 (CYP17A1) mRNA levels in the theca layer were affected and correlated with follicular androstendione and estradiol concentration. Altrenogest negatively affected follicular fluid progesterone concentration and decreased levels of prostaglandin (PG) E2 in prepubertal gilts and PGF2alpha metabolite in mature gilts. LH-stimulated cAMP release in granulosa cells of mature gilts as well as human chorionic gonadotropin- and forskolin-induced cAMP were also affected. In addition, altrenogest downregulated CYP17A1 mRNA in the prepubertal theca layer and PGF2alpha synthase expression in the granulosa and theca layer of mature gilts. To the best of our knowledge, this is the first study to report multiple effects of maturity and altrenogest on the endocrine milieu and molecular regulations governing ovarian follicle development in gilts.


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


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