scholarly journals Effects of an LH-RH analogue in male rats pretreated with oestradiol benzoate

Reproduction ◽  
1978 ◽  
Vol 54 (2) ◽  
pp. 441-445 ◽  
Author(s):  
R. K. Tcholakian ◽  
A. de la Cruz ◽  
A. K. Chowdhury ◽  
M. Chowdhury ◽  
A. V. Schally ◽  
...  
Keyword(s):  
1979 ◽  
Vol 81 (1) ◽  
pp. 35-48 ◽  
Author(s):  
B. N. PERRY ◽  
A. McCRACKEN ◽  
B. J. A. FURR ◽  
H. J. H. MACFIE

The roles of androgen and oestrogen in the perinatal and postpubertal stages of developmen on the masculinization of female patterns of growth have been investigated in several experi ments in rats. A stimulatory effect of testosterone on subsequent growth and efficiency of food utilization was only observed when administered perinatally to intact females as the propionate ester. Thus females which were untreated (or androgenized) perinatally and ovariectomized at weaning failed to grow more rapidly or utilize food more efficiently when treated with mixed testosterone esters from 36 to 38 days of age. Also autoimmunity to luteinizing hormone releasing hormone (LH-RH) had little effect on the growth or efficiency of food utilization of male rats, although testicular development was grossly affected. An inhibitory effect of oestrogen on subsequent growth and efficiency of food utilization was demonstrated by surgical ovariectomy and by autoimmunity to LH-RH. Also perinatal administration of oestradiol benzoate to intact female rats depressed growth below that of untreated intact litter-mate females until about 50 days of age. Then oestradiol benzoate-treated female rats grew to a larger size than untreated intact litter-mates but not to a heavier weight than untreated litter-mate females which like the oestradiol benzoate-treated females, were ovariectomized at 18–21 days of age. Both of these groups of female rats differed markedly in weight gain from females which were perinatally androgenized and ovariectomized at weaning. The effects of androgenization and ovariectomy on weight gain were comparable and additive in female rats fed restrictedly or ad libitum. Nevertheless, androgenized + ovariectomized female rats fed restrictedly or ad libitum failed to grow as rapidly as male rats. Some additional factor(s) prevents complete masculinization of the female pattern of development. The stimulatory effects of androgenization and ovariectomy on the growth of females appear to be related to endocrine mechanisms controlling the onset of pubertal changes in somatic development.


1981 ◽  
Vol 96 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Mridula Chowdhury ◽  
Robert Tcholakian ◽  
Emil Steinberger

Abstract. It has been suggested that treatment of intact male rats with oestradiol benzoate (OeB) causes an interference with testosterone (T) production by the testes by a direct inhibitory effect on steroidogenesis. To test this hypothesis, different doses (5, 10 or 25 IU) of hCG were administered concomitantly with 50 μg of OeB to adult intact or hypophysectomized male rats. The testicular and plasma testosterone, and serum hCG levels were determined. The sex accessory weights were recorded. In the intact OeB-treated group of animals, hCG stimulated both the secondary sex organs and plasma testosterone levels above the intact control group. However, in hypophysectomized animals, although plasma testosterone levels increased above that of intact controls, their secondary sex organ weights did not. Moreover, inspite of high circulating hCG levels, the testicular testosterone content and concentration remained suppressed in OeB-treated animals. The reason for such dichotomy of hCG action on OeB-treated animals is not clear at present.


1974 ◽  
Vol 142 (2) ◽  
pp. 273-277 ◽  
Author(s):  
Jan-Åke Gustafsson ◽  
Åke Pousette

The regulatory mechanisms involved in the control of the nuclear NADPH-dependent 3-ketosteroid 5α-reductase (5α-reductase) activity were studied in liver, kidney and prostate. The substrate used was [1,2-3H]androst-4-ene-3,17-dione (androstenedione) (for liver and kidney) or [4-14C]androstenedione (for prostate). The hepatic nuclear 5α-reductase activity was greater in female than in male rats, was greater in adult than in prepubertal female rats, increased after castration of male rats, but was not affected by treatment with testosterone propionate or oestradiol benzoate. These regulatory characteristics are in part different from those previously described for the hepatic microsomal 5α-reductase. The renal nuclear metabolism of androstenedione, i.e. 5α reduction and 17β-hydroxy steroid reduction, was relatively unaffected by sex, age, castration and treatment with testosterone propionate. However, treatment of castrated male rats with oestradiol benzoate led to a significant increase in the 5α-reductase activity and a significant decrease in the 17β-hydroxy steroid reductase activity. Finally, the nuclear 5α-reductase activity in prostate was androgen-dependent, decreasing after castration and increasing after treatment with testosterone propionate. In conclusion, the nuclear 5α-reductase activities in liver, kidney and prostate seem to be under the control of distinctly different regulatory mechanisms. The hypothesis is presented that whereas the prostatic nuclear 5α-reductase participates in the formation of a physiologically active androgen, 5α-dihydrotestosterone, this may not be the true function of the nuclear 5α-reductase in liver and kidney. These enzymes might rather serve to protect the androgen target sites in the chromatin from active androgens (e.g. testosterone) by transforming them into less active androgens (e.g. 5α-androstane-3,17-dione and/or 5α-dihydrotestosterone).


1977 ◽  
Vol 74 (2) ◽  
pp. 315-NP ◽  
Author(s):  
A. DANGUY ◽  
J. L. PASTEELS ◽  
F. ECTORS

A single injection of 1 mg of a complex of testosterone esters on day 5 of life was used to prepare constantly oestrous rats. Such androgenized female rats were then ovariectomized and submitted to stereotaxical implantation of 1 μg oestradiol benzoate, 5 μg testosterone isobutyrate or, as a control, 10 μg cholesterol in the anterior hypothalamic areas. The effects of the steroids on plasma and pituitary FSH and LH were assessed by radioimmunoassay. As reported previously by us in normal female and male rats, the preoptic–suprachiasmatic area (POA) was able to control synthesis and secretion of both gonadotrophins and did not lose its sensitivity to oestradiol and testosterone in androgenized rats. Evidence for enhanced prolactin secretion in androgenized rats was derived from immunofluorescence studies of the pituitary gland and from histology of the mammary glands. In this respect the condition of the androgenized females was opposite to that of the males. The present work demonstrated that stimulation of prolactin secretion in androgenized female rats resulted from oestrogen action due to permanent oestrus rather than from impairment of hypothalamo-hypophysial relationships. Indeed, prolactin stimulation was suppressed when the androgenized rats were ovariectomized and restored when they were subsequently implanted with oestradiol in the POA.


1983 ◽  
Vol 102 (2) ◽  
pp. 196-204 ◽  
Author(s):  
G. A. Schuiling ◽  
N. Pols-Valkhof ◽  
T. R. Koiter

Abstract. The LH releasing activities of LRH and the LRH-analogue buserelin® (HOE 766; (D-Ser (But)6-LRH(1–9)nona peptide-ethylamide) were compared in intact and short- and long-term castrated male rats, pre-treated (either 1 or 3 days) with oestradiol benzoate (EB) or oil. LRH and buserelin were infused iv at the constant rate of 104 ng/h for 21 h. Blood samples were taken from an intracarotid cannula. LH responses were judged on the basis of the mean maximal height of the LH concentration (MH; ng LH/ml plasma) and a parameter of total LH release, i.e. the area under the curve of LH concentrations plotted against time ('area under the curve', AUC; expressed in 'area units'). The release efficiency of LRH and buserelin, E (see for a definition: Materials and Methods), which informs on the total quantity of LH released in relation to pituitary LH content, was calculated by dividing the AUC × 100 by the pituitary LH content at the beginning of stimulation. Maximal plasma LH concentrations were observed between t= 1.5 and t=3 h after LRH and between t= 1.5 and t=9 after buserelin treatment. Both with LRH and buserelin the rise of LH secretion was greater the longer the animals were castrated and/or pre-treated with EB. The buserelin-induced LH response (with the exception of the responses induced in the EB-pre-treated, 4-weeks castrated rat) were about 2–2.5 times higher (MH) and larger (AUC) than the corresponding LRH-induced responses. The buserelin/LRH potency ratio, therefore, is about 2–2.5. EB-pre-treatment did not change the pituitary LH content. It therefore enhanced the efficiency of release of LH of both LRH and buserelin. Castration, on the other hand, caused an increase of the pituitary LH content: after 4 weeks it was raised by a factor 4. Since, however, the LH responses induced by LRH and buserelin were proportionally higher and larger, castration did not significantly change the efficiency of LH release. The results indicate that the efficiency of LH release can be changed by changes in the endocrine environment in the experimental animals, whilst for the magnitude of LH responses the pituitary LH content is also important. It is therefore suggested that the responsiveness of the pituitary gland to LRH (and agonistic analogues) is determined by (1) the state of the LH secretion mechanism and (2) the pituitary LH content.


1978 ◽  
Vol 76 (2) ◽  
pp. 193-202 ◽  
Author(s):  
A. O. DONOSO

The levels of prolactin and LH in the plasma of rats were determined at various times after intraventricular injection of histamine. Doses of 5 and 60 μg histamine (free base) in male rats, anaesthetized with ether, induced an increase in the level of prolactin in the plasma, whilst producing a slight decrease in the concentration of LH. Injection of 5 μg histamine at 14.00 h into female rats at all stages of the oestrous cycle caused prolactin to be released; the effect was greatest at oestrus and at day 1 of dioestrus. Histamine also gave rise to a marked increase in the level of LH in the plasma when administered to pro-oestrous rats, but had no effect when injected at the other stages of the oestrous cycle. The effect of histamine on the release of prolactin in ovariectomized, oestradiol benzoate: progesterone-primed (OVX,OB:P) rats was found to be dose-related, and the level of LH in the plasma was increased by as little as 1·25 μg. Pretreatment with adrenergic (phenoxybenzamine and propranolol) and cholinergic (atropine) antagonists failed to block the stimulatory effects of histamine on prolactin secretion, but pretreatment with methysergide (serotonin antagonist) increased the histamine-induced release of prolactin in male rats. Antagonists did not modify the response of prolactin to histamine in OVX,OB:P-primed rats. The histamine-induced release of LH in OVX,OB:P-primed rats was slightly reduced by pretreatment with phenoxybenzamine, propranolol and atropine, but not by methysergide. These results indicate that histamine facilitates the release of prolactin. The stimulatory action of histamine on both pro-oestrous and OVX,OB:P-primed but not male rats suggests that histamine may be involved in LH release in the rat. Results obtained in animals pretreated with transmitter antagonists, which were unable to prevent histamine-induced hormone release, suggest that the actions of this amine are not mediated by cholinergic, noradrenergic or serotonergic mechanisms.


1976 ◽  
Vol 81 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Jesus A. Vilchez-Martinez ◽  
Akira Arimura ◽  
Andrew V. Schally

ABSTRACT The effect of Actinomycin D (Act D) on the release of LH and FSH induced by LH-RH was investigated in rats. Immature male rats received an iv infusion over a period of 3–4 h or a quick iv injection of synthetic LH-RH. Infusion of LH-RH significantly increased serum LH and FSH levels at 1, 2, 3 and 4 h after the initiation of infusion. Pre-treatment with 100 μg/100 g b. w. Act D failed to affect the rise of serum LH and FSH levels 1 h after the infusion but significantly suppressed the response at 2, 3 and 4 h. The increase in serum LH and FSH levels after a quick injection of LH-RH was unaffected by pre-treatment with Act D whether the antibiotic was injected 1 or 2 h before LH-RH. The results suggest that the initial phase of the pituitary response to LH-RH does not require DNA-dependent RNA synthesis, whereas that in the later period does. RNA synthesis may be necessary only to maintain the increased secretion of both LH and FSH during a continuous stimulation with LH-RH.


1981 ◽  
Vol 6 (1) ◽  
pp. 39-46 ◽  
Author(s):  
L. Debeljuk ◽  
V. Rettori ◽  
S. Goijmana ◽  
D. H. Coy ◽  
A. V. Schally
Keyword(s):  

1981 ◽  
Vol 90 (1) ◽  
pp. 41-51 ◽  
Author(s):  
J. A. F. TRESGUERRES ◽  
A. I. ESQUIFINO

Male and female Wistar rats were made hyperprolactinaemic by grafting two pituitary glands of litter-mate donors under the kidney capsule at 30 days of age. Other animals were sham-operated at the same age to serve as controls. Plasma levels of prolactin, LH and FSH were measured by double-antibody radioimmunoassay. Basal preoperative prolactin levels of ∼ 10 ng/ml increased after the transplantation in both male and female rats, reaching values of ∼ 180 ng/ml. Levels of LH were significantly reduced in these hyperprolactinaemic rats, whereas an increase in FSH values was seen. After administration of LH releasing hormone (LH-RH) a reduced LH response was seen but there was no response of FSH to LH-RH or even a decrease in FSH values. Prolactin levels were also reduced by LH-RH injection. Although an increase in prolactin levels was observed in control animals after a challenge with oestradiol benzoate, reduced increments were seen in experimental animals. The positive feedback effect of oestradiol benzoate on LH in females was reduced in pituitary-grafted rats but a potentiation of the FSH positive feedback could be clearly detected. This study suggests a dissociation of LH and FSH regulation in hyperprolactinaemia.


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