BIOLOGICAL EFFECTS OF HUMAN URINARY FOLLICLE STIMULATING HORMONE

1970 ◽  
Vol 63 (3) ◽  
pp. 454-475 ◽  
Author(s):  
P. Petrusz ◽  
C. Robyn ◽  
E. Diczfalusy

ABSTRACT The biological effects of human follicle stimulating hormone (FSH) preparations were studied in intact immature female mice and in hypophysectomized immature female and male rats, following the complete neutralization of the luteinizing hormone (LH) content of human urinary menopausal gonadotrophin (HMG) preparations having – prior to neutralization – FSH:LH ratios ranging between 1.0 and 500.0. Neutralization of LH was achieved by the addition of rabbit anti-human chorionic gonadotrophin (HCG) sera of known anti-LH potency. The amount of anti-LH employed was 1.5 to 730 times more than that required for 100% neutralization. In intact immature female mice, such »LH-free« FSH preparations induced an increased ovarian weight, follicle stimulation, as well as a uterine weight increase. In immature hypophysectomized female rats, »LH-free« FSH preparations induced ovarian weight increase, growth and maturation of the Graafian follicles without repair of the deficient interstitial cells and without any signs of luteinization. These ovarian changes were associated with an increase in uterine weight and with vaginal cornification. In view of these data, it is concluded that human urinary FSH per se is capable of inducing oestrogen synthesis in hypophysectomized female rats. In immature hypophysectomized male rats, »LH-free« FSH preparations induced testicular enlargement without any stimulation of the testicular interstitial cells and without any growth of the ventral prostate and seminal vesicles. The same effects were obtained following a prolonged administration (3 weeks); spermiogenesis was stimulated, but no mature spermatozoa were found.

1984 ◽  
Vol 103 (3) ◽  
pp. 317-325
Author(s):  
A. K. Brar ◽  
G. Fink

ABSTRACT The effects of catechol oestradiol and catechol oestrone on the release of LH and prolactin were investigated in immature male and female Wistar rats. In male rats both catechol oestradiol and catechol oestrone significantly increased the plasma concentration of LH, and catechol oestradiol but not catechol oestrone significantly increased the plasma concentration of prolactin and decreased the pituitary concentration of LH. The parent oestrogens, oestradiol-17β and oestrone, had no effect on plasma LH concentrations, but both increased significantly the plasma concentration of prolactin, and oestrone but not oestradiol-17β increased the pituitary concentration of LH. In immature female rats, catechol oestradiol inhibited the surge of LH and the increase in uterine weight induced by injecting pregnant mare serum gonadotrophin (PMSG). The injection of oestrone induced an increase in the plasma concentration of LH which was about nine times greater than that produced by oestradiol-17β. There were no significant differences in the effects of these steroids on plasma prolactin concentration. These results (i) confirm that in the immature male rat catechol oestrogens can stimulate LH release and show that catechol oestradiol can increase prolactin release, (ii) show that catechol oestradiol can inhibit the stimulatory effects of PMSG on LH release and uterine weight in the immature female rat, and (iii) demonstrate that oestrone can stimulate LH release in the immature female rat. J. Endocr. (1984) 103, 317-325


1969 ◽  
Vol 60 (1) ◽  
pp. 137-156 ◽  
Author(s):  
C. Robyn ◽  
P. Petrusz ◽  
E. Diczfalusy

ABSTRACT The follicle stimulating hormone (FSH)-like activity of human chorionic gonadotrophin (HCG) preparations was assayed by the method based on the ovarian weight augmentation in intact immature rats. The potencies ranged from 4.8 to 7.4 IU equivalents of FSH per mg. The FSH-like potency of the Second International Standard Preparation of HCG was 8.5 IU per vial. However, when in intact immature rats the ovarian weight response to HCG preparations was compared at a wide range of doses (40 to 51 200 IU) to that obtained with a human menopausal gonadotrophin (HMG) preparation (0.5 to 128 IU of FSH) in the presence of 40 IU of HCG, significant differences were found. The assays conducted in hypophysectomised immature female rats were invalid, because of lack of parallelism. Antisera were prepared by immunising rabbits with HCG and human hypophysial gonadotrophin (HHG) preparations and the antigonadotrophin profiles (HCG-, FSH- and FSH-like neutralising potencies) of these antisera were established by the use of statistically valid bioassay procedures. The anti-HCG and anti-HHG sera neutralised the FSH activity of HMG preparations as well as the FSH-like activity of HCG preparations. However, 3 to 175 times more antiserum was required to neutralise the equivalent of 1.0 IU of FSH-like activity present in HCG than expected on the basis of the anti-FSH potency of the antisera. On the other hand, there was a high degree of correlation between the neutralising potencies of the antisera when tested against the FSH-like activity and the HCG activity of various HCG preparations. When the FSH-like activity of an HCG preparation was quantitatively neutralised with an anti-HCG serum, some 30 per cent of the HCG activity remained unneutralised, as evidenced by repeated bioassays. Although at least 2000 IU of this »FSH-free« HCG was administered to groups of intact as well as hypophysectomised immature female rats, this high dose of HCG did not induce an increase in ovarian weight beyond that elicited by 40 IU of untreated HCG. Histological examination of the ovaries indicated lack of follicle stimulation in the hypophysectomised, but not in the intact immature animals. There was an excessive stimulation of the interstitial cells in both types of animals. The data indicate that the FSH-like activity of HCG preparations is neither due to a contamination by FSH of pituitary origin, nor is it an evenly distributed intrinsic property of the HCG molecules. It is also concluded that the gonadotrophic activity of biologically pure HCG in immature hypophysectomised female rats consists of a specific stimulation of the interstitial cell apparatus. Such HCG preparations do not induce any follicle stimulation, not even when administered in excessive doses.


1969 ◽  
Vol 45 (1) ◽  
pp. 29-36 ◽  
Author(s):  
R. H. NAQVI ◽  
D. C. JOHNSON

SUMMARY An increase in ovarian weight in immature rats after the injection of chorionic gonadotrophin (HCG) was used to measure variations in endogenous follicle-stimulating hormone (FSH) after steroid treatment. A single injection of several steroids (testosterone, androstenediol, androstenedione, oestradiol benzoate) given 12–96 hr. before treatment with HCG caused a 30–200% increase in ovarian weight. This was not a direct effect of the steroids since hypophysectomy abolished the response, and administration of the compounds concurrently with HCG was ineffective. Within certain limits an increase in the duration of pretreatment enhanced the ovarian response while an increase in the dose of steroid had little effect. Pretreatment with testosterone propionate did not change pituitary FSH activity, indicating that the increase in circulating FSH was due to an increased production of hormone. On the other hand, pituitary FSH in animals treated with oestradiol benzoate was significantly lowered within 72 hr. suggesting an increased release of FSH.


1972 ◽  
Vol 54 (2) ◽  
pp. 277-284 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS

SUMMARY Electrical stimulation of the hypothalamus with biphasic pulses was performed in immature female rats. When performed at 27 days of age or later, electrical stimulation in the arcuate nucleus region advanced puberty in all animals, as did stimulation of the anterior hypothalamus at 29 days of age or later. Stimulation in younger rats did not uniformly advance puberty. The responsiveness to electrical stimulation thus seems to develop a few days earlier in the arcuate nucleus region than in the anterior hypothalamus. In a second experiment the possible involvement of follicle-stimulating hormone (FSH) in the advancement of puberty was investigated: the simplified augmented ovarian weight assay for endogenous FSH was performed in rats stimulated in the arcuate nucleus region as well as in controls. A marked increase in ovarian weight, indicating increased FSH levels, was demonstrated in all animals stimulated on day 27 or later; at earlier ages only a percentage of the stimulated animals responded. This percentage paralleled the percentage of animals that showed advancement of puberty. It is concluded that electrical stimulation in both the arcuate nucleus region and the anterior hypothalamus advances the onset of puberty. It is suggested that electrical stimulation causes increased plasma FSH levels and, in consequence, precocious puberty.


1971 ◽  
Vol 50 (4) ◽  
pp. 679-683 ◽  
Author(s):  
R. COLLU ◽  
F. FRASCHINI ◽  
L. MARTINI

SUMMARY Melatonin and 5-methoxytryptophol, the two methoxyindoles of pineal origin, were injected into a lateral ventricle of the brain of immature female rats. Treatment was started on the 25th day of age and terminated when the vagina opened. The injection of both methoxyindoles resulted in a statistically significant delay in vaginal opening. Since previous experiments had shown that melatonin specifically inhibits secretion of luteinizing hormone and that 5-methoxytryptophol specifically blocks release of follicle-stimulating hormone, the present results support the hypothesis that the onset of sexual maturation needs a balanced secretion of both gonadotrophins.


1978 ◽  
Vol 87 (2) ◽  
pp. 367-376 ◽  
Author(s):  
Linda Y. Johnson ◽  
Mary K. Vaughan ◽  
Russel J. Reiter ◽  
David E. Blask ◽  
P. Kevin Rudeen

ABSTRACT Arginine vasotocin (AVT) treatment (1 μg/injection) every two hours beginning at 06.00 h on the morning preceding expected ovulation significantly inhibited ovulation in 29-day-old immature female rats treated 2 days earlier with 30 IU of PMS. Pre-ovulatory plasma surges and pituitary decreases in LH, FSH and prolactin as measured by radioimmunoassay were not eliminated by AVT treatment. However, there appeared to be an early rise in plasma FSH in these rats and the maximum plasma LH value attained during the surge period in PMS-treated rats was elevated by AVT treatment. Arginine vasotocin significantly inhibited the increase in ovarian weight which occurs in PMS-treated rats on the day preceding ovulation and uterine weights were consistently depressed in AVT-treated rats. The results of this study indicate that AVT likely inhibits PMS-induced ovulation at the level of the ovary, although the possibility cannot be ruled out that inhibition resulted from the advancement of the plasma FSH rise. These data and other studies investigating the effects of AVT on reproduction indicate that AVT is possibly capable of acting at more than one level of the hypothalamo-hypophyseal-gonadal axis.


1977 ◽  
Vol 75 (3) ◽  
pp. 419-426 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS ◽  
P. KRAMER

The involvement of the adrenal gland in the release of gonadotrophins and the onset of puberty in female rats was studied. Two and four days after adrenalectomy (ADX) on either day 5 or 10 after birth, a significant decrease in the concentration of FSH was found; 4 days after ADX on either day 15 or 20, FSH concentrations had increased significantly compared with sham-operated and/or intact controls. However, in the rats adrenalectomized on day 15 or 20, the body weights were lower than in control rats. Relative uterine weights (mg/100 g body wt) in adrenalectomized rats never differed from those of control rats. A delay in the time at which vaginal opening and the first oestrus occurred was found in rats adrenalectomized at 20 or 25 days of age; however this delay was accompanied in these rats by a retardation in the gain in body weight. It is argued that the effects of ADX on both the release of gonadotrophins and the onset of puberty are primarily, and presumably exclusively, due to the effects on general bodily development (expressed in body weight). The lack of effect of ADX on uterine weight supports the hypothesis that 'oestrogen-like' products from the adrenal gland are not biologically active as oestrogens.


1967 ◽  
Vol 56 (1) ◽  
pp. 165-176 ◽  
Author(s):  
Donald C. Johnson

ABSTRACT Ventral prostates in hypophysectomized male parabiotic partners of intact animals were used to compare the amount of plasma luteinizing hormone (LH) in males and females of various ages. Ovarian weight, histology, and augmentation with chorionic gonadotrophin, in hypophysectomized androgenized females were used to estimate plasma follicle stimulating hormone (FSH) activity in intact adult males and females. In young animals, up to 50 days of age, males apparently have the same amount of plasma LH as females, but older cyclic females produced significantly heavier prostates in their hypophysectomized male partners than did males. The results are consistent with the interpretation that cyclic surges of LH added to a tonic level produced an average value higher for females than males. In contrast, males of all ages and particularly adults, have a significantly greater amount of circulating FSH than females.


1980 ◽  
Vol 85 (2) ◽  
pp. 307-315 ◽  
Author(s):  
M. S. BLANK ◽  
A. E. PANERAI ◽  
H. G. FRIESEN

The effects of subcutaneous injections of the opiate antagonist naloxone on the tonic and phasic secretion of prolactin and LH were studied in rats. During development, resting levels of prolactin in serum were decreased by naloxone (2·5 mg/kg body wt) on days 24,45 and 50 in female rats and on days 28,45 and 50 in male rats. In the adult, naloxone (2·5 mg/kg body wt) decreased basal levels of serum prolactin in male rats and levels during oestrus in female rats. In 25-day-old female rats, serum LH rose from resting levels within 7·5 min of naloxone administration (2·5 mg/kg body wt) and returned to pretreatment levels by 30 min, while prolactin fell by 7·5 min and remained low for as long as 60 min after treatment. Furthermore, a tenfold lower dose of naloxone (0·25 mg/kg body wt) did not raise basal levels of serum LH but still decreased resting levels of serum prolactin in immature female rats (24 days old). The effect of naloxone (2·5 mg/kg body wt) on phasic LH release was studied in 29-day-old immature female rats primed on day 27 with pregnant mare serum gonadotrophin (PMSG). In these PMSG-treated rats the onset of the prolactin surge was blunted by naloxone while it had no effect on phasic LH release. Naloxone (5 mg/kg body wt) also induced a rise in levels of serum LH in ovariectomized rats and, if administered with morphine, it reversed the short-term inhibition of LH secretion caused by morphine. However, naloxone was ineffective after pretreatment with oestradiol benzoate. These findings suggest that the responses of serum LH and prolactin to naloxone were dissociated and that oestrogens and opiate peptides may have interacted to regulate secretion of LH.


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