scholarly journals Effects of In Vivo and In Vitro Administration of Ghrelin, Leptin and Neuropeptide Mediators on Pulsatile Gonadotrophin-Releasing Hormone Secretion from Male Rat Hypothalamus Before and After Puberty

2007 ◽  
Vol 19 (3) ◽  
pp. 181-188 ◽  
Author(s):  
M. C. Lebrethon ◽  
A. Aganina ◽  
M. Fournier ◽  
A. Gérard ◽  
A. S. Parent ◽  
...  
Keyword(s):  
Hormone Secretion ◽  
Male Rat ◽  
Releasing Hormone ◽  
Rat Hypothalamus ◽  
Before And After ◽  
Gonadotrophin Releasing Hormone

HYPOTHALAMIC, PITUITARY AND TESTICULAR FUNCTION DURING SEXUAL MATURATION OF THE MALE RAT

1977 ◽  
Vol 72 (1) ◽  
pp. 17-26 ◽  
Author(s):  
A. H. PAYNE ◽  
R. P. KELCH ◽  
E. P. MURONO ◽  
J. T. KERLAN
Keyword(s):  
Dehydrogenase Activity ◽  
Sexual Maturation ◽  
Hydroxysteroid Dehydrogenase ◽  
Male Rat ◽  
Releasing Hormone ◽  
Isomerase Activity ◽  
Serum Lh ◽  
Rate Of Increase ◽  
Gonadotrophin Releasing Hormone

SUMMARY Hypothalamic content of gonadotrophin-releasing hormone (GnRH), serum LH and FSH, capacity of the testis to synthesize testosterone in vitro, and testicular 5-ene-3β-hydroxysteroid dehydrogenase-isomerase and 17β-hydroxysteroid dehydrogenase were measured in groups of rats at approximately 5 day intervals from birth to day 64 and at days 74 and 89. The capacity of the testes to synthesize testosterone in vitro was measured in the presence of a saturating dose of rat LH. Gonadotrophin-releasing hormone increased steadily from 0·17 ng per hypothalamus at birth to a maximum of 7 ng at day 52 and then remained constant. LH concentrations were highly variable and often exceeded adult values between days 10 and 32. After day 32 a steady rise was observed which reached adult values between days 37 and 42. FSH concentrations markedly increased from 255 ng/ml observed at birth and day 10 to a peak value of 1000 ng/ml at day 32. Subsequently there was a steady decline in FSH values until day 74 when the concentration returned to values found at birth. 5-ene-3β-Hydroxysteroid dehydrogenase-isomerase activity exhibited a rapid increase between days 12 and 19 followed by an even greater rate of increase between days 19 and 32 when adult levels were attained. 17β-Hydroxysteroid dehydrogenase activity was very low between birth and day 22. Enzyme activity began to increase at day 22 with a rapid increase in activity observed between days 37 and 58. The increase in capacity to synthesize testosterone closely followed the increase in 17β-hydroxysteroid dehydrogenase activity. The study demonstrates that during sexual maturation in the male rat, changes in serum LH and FSH do not reflect changes in hypothalamic GnRH. The appearance of Leydig cells as monitored by 5-ene-3β-hydroxysteroid dehydrogenase-isomerase activity precedes by approximately 20 days the increase in testicular capacity to synthesize testosterone in vitro. The latter coincides with the increase in 17β-hydroxysteroid dehydrogenase activity. These results suggest that 17β-hydroxysteroid dehydrogenase is a limiting factor in the ability of the testis to respond to LH stimulation.

Effects of crude and highly purified bovine inhibin (Mr 32 000 form) on gonadotrophin production by ovine pituitary cells in vitro: inhibin enhances gonadotrophin-releasing hormone-induced release of LH

1990 ◽  
Vol 127 (1) ◽  
pp. 149-159 ◽  
Author(s):  
S. Muttukrishna ◽  
P. G. Knight
Keyword(s):  
Primary Cultures ◽  
Suppressive Effect ◽  
Pituitary Cells ◽  
Dependent Manner ◽  
Α Subunit ◽  
Releasing Hormone ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone

ABSTRACT Primary cultures of ovine pituitary cells (from adult ewes) were used to investigate the actions of steroid-free bovine follicular fluid (bFF) and highly-purified Mr 32 000 bovine inhibin on basal and gonadotrophin-releasing hormone (GnRH)-induced release of FSH and LH. Residual cellular contents of each hormone were also determined allowing total gonadotrophin content/well to be calculated. As in rats, both crude and highly purified inhibin preparations promoted a dose (P < 0·001)- and time (P < 0·001)-dependent suppression of basal and GnRH-induced release of FSH as well as an inhibition of FSH synthesis, reflected by a fall in total FSH content/well. However, while neither inhibin preparation affected basal release of LH or total LH content/well, GnRH-induced LH release was significantly (P< 0·001) increased by the presence of either bFF (+ 75%) or highly-purified inhibin (+ 64%) in a dose- and time-dependent manner. This unexpected action of bFF on GnRH-induced LH release was abolished in the presence of 5 μl specific anti-inhibin serum, confirming that the response was indeed mediated by inhibin. Furthermore, neither oestradiol-17β (1 pmol/l–10 nmol/l) nor monomeric α-subunit of bovine inhibin (2·5–40 ng/ml) significantly affected basal or GnRH-induced release of LH. These in-vitro findings for the ewe lend support to a number of recent in-vivo observations and indicate that, in addition to its well-documented suppressive effect on the synthesis and secretion of FSH, inhibin may actually facilitate LH release in this species, in marked contrast to its action in the rat. Journal of Endocrinology (1990) 127, 149–159

scholarly journals Effect of exogenous glucocorticoid on osmotically stimulated antidiuretic hormone secretion and on water reabsorption in man

2006 ◽  
Vol 155 (6) ◽  
pp. 845-848 ◽  
Author(s):  
Volker Bähr ◽  
Norma Franzen ◽  
Wolfgang Oelkers ◽  
Andreas F H Pfeiffer ◽  
Sven Diederich
Keyword(s):  
Antidiuretic Hormone ◽  
Water Deprivation ◽  
Hormone Secretion ◽  
Water Reabsorption ◽  
Glucocorticoid Treatment ◽  
Osmotic Stimulation ◽  
Before And After ◽  
Stimulation Of

Objective: Glucocorticoids exert tonic suppression of antidiuretic hormone (ADH) secretion. Hypocortisolism in secondary adrenocortical insufficiency can result in a clinical picture similar to the syndrome of inappropriate ADH secretion. On the other hand, in vitro and in vivo results provide evidence for ADH suppression in states of hypercortisolism. To test the hypothesis that ADH suppression is of relevance during glucocorticoid therapy, we investigated the influence of prednisolone on the osmotic stimulation of ADH. Design and methods: Seven healthy men were subjected to water deprivation tests with the measurement of plasma ADH (pADH) and osmolality (posmol) before and after glucocorticoid treatment (5 days 30 mg prednisolone per day). Results: Before glucocorticoid treatment, the volunteers showed a normal test with an adequate increase of pADH (basal 0.54 ± 0.2 to 1.9 ± 0.72 pg/ml (mean ± S.D.)) in relation to posmol(basal 283.3 ± 8.5 to 293.7 ± 6 mosmol/kg). After prednisolone intake, pADH was attenuated (<0.4 pg/ml) in spite of an increase of posmol from 289.3 ± 3.6 to 297.0 ± 5.5 mosmol/kg. However, urine osmolar concentration increased normally during water deprivation after prednisolone. Urinary cAMP excretion increased during water deprivation without glucocorticoid treatment from 3.56 ± 0.55 to 6.07 ± 0.76 μmol/l, reflecting the increased pADH levels. The rise in cAMP excretion was completely blunted by prednisolone treatment. Conclusions: We speculate that there may be an ADH-independent stimulation of the formation or function of aquaporin-2 channels by prednisolone and/or a direct osmotic stimulation of water reabsorption independent of ADH and glucocorticoid control.

Effect of chronic exposure to a gonadotrophin-releasing hormone agonist on in vitro responsiveness of ovine pituitary cells to inhibin, activin and oestradiol

1994 ◽  
Vol 140 (3) ◽  
pp. 483-493 ◽  
Author(s):  
S Muttukrishna ◽  
P G Knight
Keyword(s):  
Gnrh Agonist ◽  
Inhibitory Effect ◽  
Pituitary Cells ◽  
Cell Content ◽  
Releasing Hormone ◽  
Basal Release ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone

Abstract To investigate the extent to which the direct actions of inhibin, activin and oestradiol on pituitary output of FSH and LH are dependent on the presence of functional gonadotrophin-releasing hormone (GnRH) receptors, we have compared the effects of these agents on cultured ovine pituitary cells derived from control and GnRH agonist-suppressed ewes. Chronic treatment with GnRH agonist reduced plasma LH and FSH levels (P<0·01) and abolished GnRH-induced release of LH and FSH both in vivo and in vitro. As expected, basal LH release and LH cell content in vitro were drastically reduced in GnRH agonist-suppressed cells (P<0·001). However, basal FSH release and FSH cell content were approximately twofold higher than in control cells (P<0·001). Irrespective of whether the cells had been desensitized to GnRH, inhibin and oestradiol were both found to suppress basal FSH release and FSH cell content in a dose-dependent fashion (P<0·001). Although inhibin had no effect on basal release of LH from control cells, it markedly enhanced GnRH-induced release (P<0·001). In contrast, inhibin increased (P<0·001) basal LH release from GnRH agonist-suppressed cells (which were unresponsive to the GnRH challenge). Inhibin had no overall effect on total LH content/well for either control or GnRH agonist-suppressed cells. Treatment with oestradiol, on the other hand, reduced total LH content/well, an effect which was more pronounced with GnRH agonist-suppressed cells (−44%; P<0·001) than with control cells (−14%, P<0·01). Whereas in control cells activin had no significant effect on any aspect of FSH production examined, in GnRH agonist-treated cells activin enhanced basal FSH release, residual cell content and total FSH content/well (P<0·001). Altering GnRH receptor status also modified the LH response to activin. With control cells activin increased basal release (P<0·001), decreased GnRH-induced release (P<0·001) and increased total LH content/well (P<0·001). With GnRH agonist-treated cells, however, activin had a uniform inhibitory effect on each aspect of LH production examined (P<0·001 in each case). It was concluded that desensitization of ovine gonadotrophs to GnRH by chronic agonist treatment results in a paradoxical enhancement of FSH output in vitro but has little effect on the responsiveness of the cells (in terms of gonadotrophin release and content) to either inhibin or oestradiol. In contrast, GnRH agonist treatment leads to qualitative changes in cellular reponsiveness to activin. Journal of Endocrinology (1994) 140, 483–493

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