Inhibitory Control of the Pituitary LH Secretion by LH-RH in Male Rats

1979 ◽  
Vol 11 (6) ◽  
pp. 303-317 ◽  
Author(s):  
J. Sandow ◽  
W.v. Rechenberg ◽  
H. Kuhl ◽  
R. Baumann ◽  
B. Krauss ◽  
...  
Keyword(s):  
Inhibitory Control ◽  
Male Rats ◽  
Lh Rh ◽  
Lh Secretion

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):  
Male Rats ◽  
Oestradiol Benzoate ◽  
Lh Rh

Orchidectomy selectively increases follicle-stimulating hormone secretion in gonadotropin-releasing hormone antagonist-treated male rats

1995 ◽  
Vol 132 (3) ◽  
pp. 357-362 ◽  
Author(s):  
M Tena-Sempere ◽  
L Pinilla ◽  
E Aguilar
Keyword(s):  
Gnrh Antagonist ◽  
Follicle Stimulating Hormone ◽  
Hormone Secretion ◽  
Gonadotropin Releasing Hormone ◽  
Male Rats ◽  
Gonadotropin Secretion ◽  
Releasing Hormone ◽  
Treated Male ◽  
Lh Secretion ◽  
Stimulating Hormone

Tena-Sempere M, Pinilla L, Aguilar E. Orchidectomy selectively increases follicle-stimulating hormone secretion in gonadotropin-releasing hormone agonist-treated male rats. Eur J Endocrinol 1995;132: 357–62. ISSN 0804–4643 The pituitary component of the feedback mechanisms exerted by testicular factors on gonadotropin secretion was analyzed in adult male rats treated with a potent gonadotropin-releasing hormone (GnRH) antagonist. In order to discriminate between androgens and testicular peptides, groups of males were orchidectomized (to eliminate androgens and non-androgenic testicular factors) or injected with ethylene dimethane sulfonate (EDS), a selective toxin for Leydig cells (to eliminate selectively androgens) and treated for 15 days with vehicle or the GnRH antagonist Ac-d-pClPhe-d-pClPhe-d-TrpSer-Tyr-d-Arg-Leu-Arg-Pro-d-Ala-NH2CH3COOH (Org.30276, 5 mg/kg/72 hours). Serum concentrations of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured 7 and 14 days after the beginning of treatment. We found that: in males treated with GnRH antagonist, orchidectomy or EDS treatment did not induce any increase in LH secretion; and orchidectomy, but not EDS treatment, increased FSH secretion in GnRH-treated males. The present results show that negative feedback of testicular factors on LH secretion is mediated completely through changes in GnRH actions. In contrast, a part of the inhibitory action of the testis on FSH secretion is exerted directly at the pituitary level. It can be hypothesized that non-Leydig cell testicular factor(s) inputs at different levels of the hypothalamic–pituitary axis in controlling LH and FSH secretion. Manuel Tena-Sempere, Department of Physiology, Faculty of Medicine, University of Córdoba, 14004 Córdoba, Spain

LH SECRETION DURING LONG-TERM EXPOSURE OF PITUITARY GLANDS TO LH-RH

1981 ◽  
pp. 65-71
Author(s):  
G.P. van Rees ◽  
J.A.M.J. van Dieten ◽  
A.M.I. Tijssen ◽  
J. de Koning
Keyword(s):  
Pituitary Glands ◽  
Lh Rh ◽  
Lh Secretion

INHIBITION BY MELATONIN OF THE PITUITARY RESPONSE TO LUTEINIZING HORMONE RELEASING HORMONE IN VIVO

1978 ◽  
Vol 76 (3) ◽  
pp. 487-491 ◽  
Author(s):  
K. YAMASHITA ◽  
M. MIENO ◽  
T. SHIMIZU ◽  
ER. YAMASHITA
Keyword(s):  
Luteinizing Hormone ◽  
Carotid Artery ◽  
Anterior Pituitary ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Lh Secretion

The rate of secretion of 17-oxosteroids by the testes of anaesthetized dogs in vivo was used as an index of LH secretion. Intracarotid injection of luteinizing hormone releasing hormone (LH-RH, 1, 5 or 10 μg/kg body wt) resulted in an increase in the testicular 17-oxosteroid secretion which was roughly proportional to the dose administered and which reached a maximum 60 min after the injection. Testicular output of 17-oxosteroids was unaffected by administration of melatonin (10 or 100 μg/kg body wt) into the carotid artery. When LH-RH (5 μg/kg) was injected into the carotid artery 3 h after intracarotid injection of melatonin (10 or 100 μg/kg), the testicular response to LH-RH was considerably diminished. Pretreatment with melatonin (100 μg/kg) did not alter the testicular response to human chorionic gonadotrophin (20 i.u./kg body wt) given i.v. It is concluded that melatonin may act directly on the anterior pituitary gland in dogs to inhibit the LH-RH-induced release of LH.

Immunocytochemical studies on effects of LHRH on pituitary LH secretion in male rats

Contraception ◽  
1992 ◽  
Vol 46 (2) ◽  
pp. 163-165
Author(s):  
Shou-kang Zhou ◽  
Chung-ming Hsieh ◽  
Wein-yen Lu
Keyword(s):  
Male Rats ◽  
Immunocytochemical Studies ◽  
Lh Secretion

LH-RH Neurones: Neurophysiology of Hypothalamic Control of LH Secretion

2015 ◽  
pp. 176-182 ◽  
Author(s):  
R. G. Dyer ◽  
Sandra Mansfield ◽  
J. O. Yates
Keyword(s):  
Hypothalamic Control ◽  
Lh Rh ◽  
Lh Secretion

Comparison of the LH secretion patterns in the male rat following infusion of LRH and of the LRH-analogue buserelin®. Influence of castration and oestradiol benzoate on the efficiency of LH release

1983 ◽  
Vol 102 (2) ◽  
pp. 196-204 ◽  
Author(s):  
G. A. Schuiling ◽  
N. Pols-Valkhof ◽  
T. R. Koiter
Keyword(s):  
Area Under The Curve ◽  
Male Rats ◽  
Male Rat ◽  
Potency Ratio ◽  
Maximal Height ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Buserelin Treatment ◽  
Pre Treatment ◽  
Lh Secretion

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.

EFFECT OF ACTINOMYCIN D ON THE PITUITARY RESPONSE TO LH-RH

1976 ◽  
Vol 81 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Jesus A. Vilchez-Martinez ◽  
Akira Arimura ◽  
Andrew V. Schally
Keyword(s):  
Initial Phase ◽  
Rna Synthesis ◽  
Actinomycin D ◽  
Male Rats ◽  
Continuous Stimulation ◽  
Immature Male ◽  
Serum Lh ◽  
Pre Treatment ◽  
Lh Rh

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.

Mechanisms of altered LH secretion in neonatally oestrogenized male rats

1995 ◽  
Vol 147 (1) ◽  
pp. 43-50 ◽  
Author(s):  
L Pinilla ◽  
M Tena-Sempere ◽  
D Gonzalez ◽  
E Aguilar
Keyword(s):  
Leydig Cells ◽  
Postnatal Period ◽  
Male Rats ◽  
Control Groups ◽  
Gonadotrophin Secretion ◽  
Selective Elimination ◽  
Lhrh Release ◽  
Lh Secretion

Abstract It is well known that the control of LH secretion depends on the steroid milieu during the postnatal period. In this study LH secretion was analysed in adult male rats injected neonatally with 500 μg oestradiol benzoate (1) after orchidectomy, (2) after selective elimination of androgens by destruction of Leydig cells with ethylene dimethane sulphonate (EDS), and (3) after removal in orchidectomized animals of Silastic capsules containing testosterone. In addition, (4) in vivo and in vitro LH secretion in response to LHRH agonist and antagonists, (5) the hypothalamic LHRH content, (6) the basal and stimulated in vitro LHRH release, and (7) the LH responses after administration of naloxone (2 mg/kg), α-methyl-p-tyrosine (α-MPT; 250 mg/kg), N-methyl-d-aspartic acid (NMDA, 15 mg/kg) or kainic acid (KA; 15 mg/kg) were also examined. Our data indicated that (1) the LH response after orchidectomy, after EDS administration and after removal of Silastic capsules containing testosterone was diminished in oestrogenized male rats, (2) the pituitaries from oestrogenized males retained responsiveness to LHRH, (3) hypothalamic LHRH content was reduced in oestrogenized males, but the hypothalamus from oestrogenized males released more LHRH than those of control groups both under basal conditions or after depolarization, (4) α-MPT decreased LH secretion only in oestrogenized males, and (5) NMDA and KA stimulated LH only in oestrogenized males. We conclude that in oestrogenized male rats the loss of sensitivity to the negative feedback action of testosterone on LH secretion was not due to decreased pituitary responsiveness to LHRH stimulation or to the inherent damage of LHRH neurones. In contrast, changes in the mechanisms governing LHRH release seem to be involved. A lack of activation of the excitatory noradrenergic and aminoacidergic systems seems to be part of the neurochemical basis of altered gonadotrophin secretion in neonatally oestrogenized male rats. Journal of Endocrinology (1995) 147, 43–50

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