Pituitary-Testicular Function in Protein-Deficient Rats. Follicle-Stimulating Hormone Hyperresponse to Castration and Supersensitivity of Gonadotropin Secretion to Androgen Negative Feedback*

Endocrinology ◽  
1982 ◽  
Vol 110 (5) ◽  
pp. 1542-1546 ◽  
Author(s):  
ALLAN R. GLASS ◽  
ANNA STEINBERGER ◽  
RONALD SWERDLOFF ◽  
ROBERT A. VIGERSKY
Keyword(s):  
Negative Feedback ◽  
Follicle Stimulating Hormone ◽  
Testicular Function ◽  
Gonadotropin Secretion ◽  
Stimulating Hormone

Responses of luteinizing hormone (LH) and follicle-stimulating hormone levels to exogenous gonadotropin-releasing hormone during the estrogen-induced LH surge in the ovariectomized rhesus monkey

1989 ◽  
Vol 67 (2) ◽  
pp. 135-139 ◽  
Author(s):  
Richard F. Weick ◽  
Vaclav Pitelka ◽  
David L. Thompson
Keyword(s):  
Luteinizing Hormone ◽  
Rhesus Monkey ◽  
Negative Feedback ◽  
Follicle Stimulating Hormone ◽  
Gonadotropin Releasing Hormone ◽  
Gonadotropin Secretion ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Acute Response ◽  
Stimulating Hormone

Experiments were performed to study the responsiveness of the pituitary to gonadotropin-releasing hormone (GnRH) during the dynamic changes in gonadotropin secretion associated with the estrogen-induced luteinizing hormone (LH) surge in the ovariectomized (OVX) rhesus monkey. Silastic capsules filled with estradiol-17-β were implanted subcutaneously in ovariectomized rhesus monkeys, resulting in an initial lowering of circulating LH and follicle-stimulating hormone (FSH) concentrations followed by an LH–FSH surge. GnRH was injected intravenously just before estrogen implantation, during the negative feedback response and during the rising, the peak, and the declining phases of the LH surge. The LH and FSH responses during the negative feedback phase were as large as those before estrogen treatment (control responses). During the rising phase of the LH surge, the acute response to GnRH injection did not differ significantly from the control response, but the responses 60 and 120 min after injection were somewhat increased. During the declining phase of the LH surge, the pituitary was not responsive to exogenous GnRH, although LH probably continued to be secreted at this time since the LH surge decreased more slowly than predicted by the normal rate of disappearance of LH in the monkey. We conclude that an increased duration of response to GnRH may be an important part of the mechanism by which estrogen induces the LH surge, but we do not see evidence of increased sensitivity of the pituitary to GnRH as an acute releasing factor at that time.Key words: LH surge, GnRH, FSH, ovariectomized monkey.

Studies on Spermatogenesis in Rats. III. Effects of Hormonal Treatment on Differentiation Kinetics of the Spermatogenic Cycle in Regressed Hypophysectomized Rats

1971 ◽  
Vol 49 (7) ◽  
pp. 768-775 ◽  
Author(s):  
V. L. W. Go ◽  
R. G. Vernon ◽  
I. B. Fritz
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Hormonal Treatment ◽  
Testicular Function ◽  
Carnitine Acetyltransferase ◽  
Hormonal Replacement ◽  
Hypophysectomized Rats ◽  
Kinetics Of ◽  
Stimulating Hormone

The general hormonal requirements for the restoration of spermatogenesis in regressed hypophysectomized rats were investigated. With the aid of the Staput fractionation technique, it was established that thymidine-3H was readily incorporated into spermatogonia and resting spermatocytes. Labeled cells did not progress to form appreciable numbers of primary spermatocytes or spermatids in the absence of hormonal replacement. The inhibition of formation of pachytene primary spermatocytes in hypophysectomized rats was overcome by administration of follicle-stimulating hormone (FSH), luteinizing hormone (LH), or testosterone, but a combination of either FSH plus LH, or FSH plus testosterone, was required for the progression of pachytene primary spermatocytes to spermatids and spermatozoa. Carnitine acetyltransferase (CAT) measurements in testes from various groups of animals provided ancillary evidence consistent with the conclusion that either FSH, LH, or testosterone was required for the normal restoration of pachytene-diplotene spermatocyte formation. However, one or more additional blocks in spermatogenesis existed in hypophysectomized animals, since elevation of depressed testicular CAT levels in hypophysectomized rats to normal levels required FSH plus LH, or FSH plus testosterone. Cortisone and thyroxin treatment had no measurable effects on testicular function in hypophysectomized rats.

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

Endocrine and local testicular regulation

2011 ◽  
pp. 1347-1353
Author(s):  
Ilpo Huhtaniemi
Keyword(s):  
Growth Factors ◽  
Luteinizing Hormone ◽  
Leydig Cell ◽  
Follicle Stimulating Hormone ◽  
Regulatory System ◽  
The Other ◽  
Seminiferous Tubules ◽  
Testicular Function ◽  
Cell Product ◽  
Stimulating Hormone

The testis has two functions, androgen production and spermatogenesis, and a key role in their regulation is played by the two pituitary gonadotropins, luteinizing hormone and follicle-stimulating hormone (FSH). Other hormones and growth factors also influence testicular function, often by modulating the gonadotropin effects. Moreover, a plethora of local paracrine and autocrine signals within the testis are known. The main testicular hormone, testosterone, a Leydig cell product, regulates spermatogenesis in seminiferous tubules in paracrine fashion. The other functions of testosterone are endocrine, occurring outside the testis. This chapter summarizes the main hormonal regulatory system of the testis, the hypothalamic–pituitary–testicular axis, and how its effects are modulated by other extratesticular hormones and local testicular factors.

Chronic Nitric Oxide Deficiency is Associated with Altered Leutinizing Hormone and Follicle-Stimulating Hormone Release in Ovariectomized Rats1

2002 ◽  
Vol 227 (9) ◽  
pp. 817-822 ◽  
Author(s):  
Maria J. Barnes ◽  
Karen Lapanowski ◽  
Jose A. Rafols ◽  
David M. Lawson ◽  
Joseph C. Dunbar
Keyword(s):  
Nitric Oxide ◽  
Follicle Stimulating Hormone ◽  
Independent Effect ◽  
Control Group ◽  
Gonadotropin Secretion ◽  
No Donor ◽  
Ovx Rats ◽  
Nos Inhibitor ◽  
Stimulating Hormone

Nitric oxide (NO) synthase (NOS) has been found in the gonadotrophs and folliculo-stellate cells of the anterior pituitary. Previous observations from our laboratory suggest that NO may play a role in regulating gonadotropin secretion. Because estrogen secretion by the ovary can influence gonadotropin secretion, we investigated the hypothesis that chronic in vivo NO deficiency has a direct estrogen-independent effect on luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. Chronic NO deficiency was induced by adding an NOS inhibitor, N-nitro-L-arginine (L-NNA, 0.6 g/l) to the drinking water of ovariectomized (OVX) rats. The control OVX rats were untreated. After 6–8 weeks, the animals were sacrificed, and the pituitaries were removed and perfused continuously for 4 hr in the presence of pulsatile gonadotropin-releasing hormone (GnRH, 500 ng/pulse) every 30 min. S-Nitroso-l-acetyl penicillamine (SNAP, an NO donor, 0.1 mM) or l-nitro-arginine methyl ester (L-NAME, an NOS inhibitor, 0.1 mM) was added to the media and perfusate samples were collected at 10-min intervals. GnRH-stimulated LH and FSH levels were significantly lower in pituitaries from OVX/NO-deficient pituitaries compared with pituitaries from the OVX control group. The addition of SNAP significantly decreased LH and FSH secretion by pituitaries from OVX control animals, but significantly increased their secretion by pituitaries from the OVX/NO-deficient animals. L-NAME also suppressed LH and FSH secretion by pituitaries from the OVX control animals and stimulated their release by pituitaries from the NO-deficient/OVX animals. Immunohisto-chemistry of frontal sections through the hypothalamus demonstrated that OVX/NO deficiency is associated with increased GnRH in the median eminence. We conclude that NO has a chronic stimulatory effect on LH and FSH release and the subsequent altered secretory responsiveness to NO agonist or antagonist is the result of chronic NO suppression.

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