Potentiation of prostaglandin E2-induced release of LH by the prostaglandin analogue, 7-oxa-13-prostynoic acid

1981 ◽  
Vol 97 (3) ◽  
pp. 297-304
Author(s):  
Jørgen Warberg
Keyword(s):  
Binding Site ◽  
Hormone Secretion ◽  
Male Rats ◽  
Stimulatory Action ◽  
Minimal Effective Dose ◽  
Lh Release ◽  
Pre Treatment ◽  
Intraventricular Infusion ◽  
The Brain ◽  
Stimulation Of

Abstract. The prostaglandin (PG) analogue 7-oxa-13-prostynoic acid (7-OPA) was infused into a lateral ventricle of the brain of adult male rats and the effect of the analogue on a subsequent stimulation of LH release by intraventricular infusion of PG's was determined. Pre-treatment of the animals with 44–132 μg of 7-OPA potentiated the stimulatory effect of 2 μg PGE2 on the release of LH but the analogue alone had no effect on the hormone secretion. The minimal effective dose of PGE2 was determined to be within the range 0.01–0.05 μg and it was found that priming with 132 μg of 7-OPA caused a formerly sub-threshold dose (0.01 μg) of PGE2 to become an effective stimulus for the release of LH. In contrast to its potentiating effect on PGE2-induced LH release 7-OPA did not alter the stimulatory action of PGF2α (2 μg) on the secretion of LH. 7-OPA had no effect on LRH-induced release of LH indicating that the PG analogue acts at a suprapituitary site to enhance PGE2-induced LH release. The potentiating effect of 7-OPA may be exerted at a binding site for PGE2 in the brain and the results suggest the existence of a different binding site for PGF2α. The possibility also exists that 7-OPA inhibit metabolic inactivation of PGE2.

Differential effects of passive immunization with somatostatin antiserum on adenohypophysial hormone secretions in starved rats

1986 ◽  
Vol 109 (2) ◽  
pp. 169-174 ◽  
Author(s):  
J. N. Hugues ◽  
A. Enjalbert ◽  
E. Moyse ◽  
C. Shu ◽  
M. J. Voirol ◽  
...  
Keyword(s):  
Binding Capacity ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Passive Immunization ◽  
Negative Control ◽  
Prolactin Secretion ◽  
Male Rats ◽  
Minimal Effective Dose ◽  
Gh Secretion

ABSTRACT The role of somatostatin (SRIF) on adenohypophysial hormone secretion in starved rats was reassessed by passive immunization. Because of the absence of pulsatile GH secretion in starved rats, the effects of the injection of SRIF antiserum on GH levels can be clearly demonstrated. To determine whether starvation modifies the sensitivity of the adenohypophysis to SRIF, we measured 125I-labelled iodo-N-Tyr-SRIF binding. There was no difference in the dissociation constant (Kd) nor in the maximal binding capacity (Bmax) in fed (n = 15) and starved (n = 15) animals (Kd = 0·38 ± 0·09 (s.e.m.) and 0·45 ± 0·09 nmol; Bmax = 204 ± 39 and 205 ± 30 fmol/mg protein respectively). Administration of SRIF antiserum resulted in a dose-dependent increase in plasma concentrations of GH, TSH and prolactin. The minimal effective dose of SRIF antiserum was 50 μl for GH, 100 μl for TSH and 200 μl for prolactin. Our results show that: (1) starvation does not modify adenohypophysial SRIF-binding sites, (2) in starved male rats endogenous SRIF exerts a negative control on prolactin secretion in vivo and (3) sensitivity to endogenous SRIF seems to be different for each hypophysial cell type. J. Endocr. (1986) 109, 169–174

scholarly journals Obestatin Partially Affects Ghrelin Stimulation of Food Intake and Growth Hormone Secretion in Rodents

Endocrinology ◽  
2007 ◽  
Vol 148 (4) ◽  
pp. 1648-1653 ◽  
Author(s):  
Philippe Zizzari ◽  
Romaine Longchamps ◽  
Jacques Epelbaum ◽  
Marie Thérèse Bluet-Pajot
Keyword(s):  
Food Intake ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Male Rats ◽  
Pituitary Cells ◽  
Gh Secretion ◽  
Freely Moving ◽  
Stimulation Of

Administration of ghrelin, an endogenous ligand for the GH secretagogue receptor 1a (GHSR 1a), induces potent stimulating effects on GH secretion and food intake. However, more than 7 yr after its discovery, the role of endogenous ghrelin remains elusive. Recently, a second peptide, obestatin, also generated from proteolytic cleavage of preproghrelin has been identified. This peptide inhibits food intake and gastrointestinal motility but does not modify in vitro GH release from pituitary cells. In this study, we have reinvestigated obestatin functions by measuring plasma ghrelin and obestatin levels in a period of spontaneous feeding in ad libitum-fed and 24-h fasted mice. Whereas fasting resulted in elevated ghrelin levels, obestatin levels were significantly reduced. Exogenous obestatin per se did not modify food intake in fasted and fed mice. However, it inhibited ghrelin orexigenic effect that were evident in fed mice only. The effects of obestatin on GH secretion were monitored in superfused pituitary explants and in freely moving rats. Obestatin was only effective in vivo to inhibit ghrelin stimulation of GH levels. Finally, the relationship between octanoylated ghrelin, obestatin, and GH secretions was evaluated by iterative blood sampling every 20 min during 6 h in freely moving adult male rats. The half-life of exogenous obestatin (10 μg iv) in plasma was about 22 min. Plasma obestatin levels exhibited an ultradian pulsatility with a frequency slightly lower than octanoylated ghrelin and GH. Ghrelin and obestatin levels were not strictly correlated. In conclusion, these results show that obestatin, like ghrelin, is secreted in a pulsatile manner and that in some conditions; obestatin can modulate exogenous ghrelin action. It remains to be determined whether obestatin modulates endogenous ghrelin actions.

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.

INDUCTION OF PROLACTIN AND LUTEINIZING HORMONE RELEASE BY HISTAMINE IN MALE AND FEMALE RATS AND THE INFLUENCE OF BRAIN TRANSMITTER ANTAGONISTS

1978 ◽  
Vol 76 (2) ◽  
pp. 193-202 ◽  
Author(s):  
A. O. DONOSO
Keyword(s):  
Prolactin Secretion ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Male Rats ◽  
Intraventricular Injection ◽  
Hormone Release ◽  
Stimulatory Action ◽  
Male And Female Rats ◽  
Oestradiol Benzoate ◽  
Lh Release

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.

THE EFFECT OF VARIOUS ACTH EXTRACTS ON THE GONADS

1954 ◽  
Vol 10 (4) ◽  
pp. 291-301 ◽  
Author(s):  
R. W. BRIMBLECOMBE ◽  
I. D. K. HALKERSTON ◽  
M. REISS
Keyword(s):  
Ascorbic Acid ◽  
Female Rats ◽  
Male Rats ◽  
Stimulatory Action ◽  
Follicular Maturation ◽  
Accessory Sex Organs ◽  
Stimulation Of

SUMMARY ACTH extracts showing inhibition of the stimulatory action of PMS on follicular maturation in infantile female rats and slight stimulation of the growth of the testes and accessory sex organs in infantile male rats and day-old chicks have been investigated. The action of these extracts on the gonads was found to be independent of the adrenal ascorbic acid depleting principle, as ACTH fractions free from inhibitory or stimulatory influence on the gonads could be prepared. The nature of the factor described is discussed.

scholarly journals A Possible Mechanism for the Action of Adrenomedullin in Brain to Stimulate Stress Hormone Secretion

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 4890-4896 ◽  
Author(s):  
Meghan M. Taylor ◽  
Willis K. Samson
Keyword(s):  
Hpa Axis ◽  
Hormone Secretion ◽  
Plasma Corticosterone ◽  
Male Rats ◽  
Stress Hormone ◽  
Elevated Plasma ◽  
The Central Nervous System ◽  
Neuroendocrine Responses ◽  
The Brain

Abstract Adrenomedullin (AM) has been reported to have actions at each level of the hypothalamo-pituitary-adrenal (HPA) axis, suggesting that the peptide plays a role in the organization of the neuroendocrine responses to stress. We examined the mechanism by which AM regulates the central nervous system branch of the HPA axis as well as the possible role of AM in the modulation of the releases of two other hormones, prolactin and GH, whose secretions also are altered by stress. Intracerebroventricular administration of AM led to elevated plasma corticosterone levels in unrestrained, conscious male rats. This effect was abrogated by pretreatment with a CRH antagonist, suggesting that AM activates the HPA axis by causing the release of CRH into hypophyseal portal vessels. In addition, AM given intracerebroventricularly stimulated the release of prolactin but did not alter the secretion of GH. We propose that AM produced in the brain may be an important neuromodulator of the hormonal stress response.

Vagal regulation of gastric prostaglandin E2 release by central TRH in rats

1993 ◽  
Vol 264 (2) ◽  
pp. G231-G236 ◽  
Author(s):  
M. Yoneda ◽  
Y. Tache
Keyword(s):  
Prostaglandin E2 ◽  
Acid Output ◽  
Biologically Active ◽  
Central Action ◽  
Stimulatory Action ◽  
Pge2 Release ◽  
Cervical Vagotomy ◽  
The Brain ◽  
Stimulation Of

The central action of the stable thyrotropin-releasing hormone (TRH) analogue, RX 77368, to induce vagal release of gastric prostaglandin E2 (PGE2) was investigated in urethan-anesthetized rats. Intracisternal RX 77368 (1.5-1,000 ng) dose dependently increased gastric PGE2 levels measured for 3 h in the perfusate of dialysis fibers implanted into the corpus submucosa. RX 77368 injected intravenously (1,000 ng) had no effect. The stimulatory action of RX 77368 (1.5 ng) on gastric PGE2 release was blocked by indomethacin and bilateral cervical vagotomy. Omeprazole did not alter the PGE2 response to 3 ng of RX 77368 and reduced by 39% PGE2 release induced by the 1,000-ng dose. RX 77368 (1.5 ng) by itself did not influence acid secretion but increased acid output to 117 +/- 18 mumol/2 h in indomethacin-pretreated rats. Indomethacin also increased by 97% the acid response to the 3-ng dose of RX 77368, but the effect of a maximal effective dose of RX 77368 was not modified. These results indicate that RX 77368 acts in the brain to induce a vagal-dependent stimulation of gastric PGE2 secretion which is biologically active to reduce the acid response to submaximal doses of TRH analogue. These data suggest a possible role of medullary TRH in the central vagal regulation of gastric PGE2 release.

scholarly journals Effects of Electrical Stimulation of the Brain on Gonadotropin Secretion in Male Rats

1973 ◽  
Vol 20 (5) ◽  
pp. 447-454 ◽  
Author(s):  
MASAZUMI KAWAKAMI ◽  
FUKUKO KIMURA ◽  
TAKASHI HIGUCHI
Keyword(s):  
Electrical Stimulation ◽  
Male Rats ◽  
Gonadotropin Secretion ◽  
The Brain ◽  
Stimulation Of

PRIMING EFFECT OF LUTEINIZING HORMONE RELEASING FACTOR ELICITED BY PREOPTIC STIMULATION AND BY INTRAVENOUS INFUSION AND MULTIPLE INJECTIONS OF THE SYNTHETIC DECAPEPTIDE

1976 ◽  
Vol 69 (3) ◽  
pp. 359-372 ◽  
Author(s):  
G. FINK ◽  
S. A. CHIAPPA ◽  
M. S. AIYER
Keyword(s):  
Priming Effect ◽  
Preoptic Area ◽  
Male Rats ◽  
Constant Rate ◽  
Enhanced Secretion ◽  
The Mean ◽  
Low Levels ◽  
Pre Treatment ◽  
Electrical Stimuli ◽  
Stimulation Of

SUMMARY We have investigated whether the priming effect of LH-RF can be elicited by electrical stimulation of the medial preoptic area, or by i.v. infusion or multiple i.v. injections of the synthetic decapeptide. All experiments were carried out on animals anaesthetized with sodium pentobarbitone at 13.30 h. In pro-oestrous rats, the LH response to the second of two electrical stimuli, 15 min in duration and separated by 60 min, was significantly greater than the response to the first stimulus. When synthetic LH-RF was infused at a constant rate for 90 min, plasma LH increased gradually for the first 45–60 min after which it increased markedly. This enhanced secretion of LH did not occur in rats which were infused with the same total dose of LH-RF, either 15 or 75 ng/100 g body wt, over periods of 45 min or less. When a dose of 15 ng LH-RF/100 g body wt was administered in six divided doses by i.v. injections, each separated by 15 min, there was a marked increase in plasma LH after 75 min. The profile of the mean plasma LH concentration in rats subjected to preoptic stimulation for 90 min was similar to that in rats infused for 90 min with LH-RF, but the variation in response was much greater in the stimulated rats. These results indicate that the priming effect can be elicited by endogenous as well as synthetic LH-RF, and that whether LH-RF reaches the pituitary at a constant rate or in a pulsatile manner the factor is capable of significantly increasing the responsiveness of the gonadotrophs. The relevance of these findings with respect to the development of the spontaneous preovulatory LH surge is discussed. A priming effect could not be elicited by constant LH-RF infusion in dioestrous rats; this supports the view that steroid hormones, especially oestradiol-17β, determine the magnitude of the effect. The LH response in male rats subjected to i.v. infusion of LH-RF was much lower than in females. Pre-treatment with oestradiol benzoate did not increase the response significantly, suggesting that this sex difference cannot be ascribed simply to low levels of plasma oestrogen in the male.

PERIPHERAL AND CENTRAL ANDROGENIC STIMULATION OF SEXUAL BEHAVIOUR OF CASTRATED MALE RATS

1977 ◽  
Vol 84 (4) ◽  
pp. 813-828 ◽  
Author(s):  
Rachel Hamburger-Bar ◽  
Henk Rigter
Keyword(s):  
Sexual Behaviour ◽  
Testosterone Propionate ◽  
Male Rats ◽  
Peripheral Target ◽  
Peripheral Tissues ◽  
Target Organs ◽  
The Brain ◽  
Stimulation Of ◽  
Maintenance Study

ABSTRACT The effects of androgens on the maintenance and restoration of sexual behaviour (mounts, intromissions and ejaculations) of castrated male rats were studied. In the maintenance study the rats were treated during 5 weeks, starting one day following castration. Testosterone propionate maintained sexual behaviour at an almost normal level. The androgenoestrogen intermediate 19-hydroxytestosterone propionate was unable to prevent the decline in the number of ejaculations over the weeks although this hormone maintained the post-ejaculatory refractory period in those rats that ejaculated and also maintained normal sexual latencies. In the restoration study administration of testosterone propionate during 7 weeks to long-term castrated rats restored sexual behaviour to normal. 19-Hydroxytestosterone propionate treated rats displayed mounts but no other signs of sexual behaviour. The 5α-reduced androgen dihydrotestosterone propionate did not restore sexual behaviour. Testosterone propionate and dihydrotestosterone propionate stimulated peripheral target organs; 19-hydroxytestosterone propionate was ineffective in this respect. It has been suggested that testosterone might stimulate sexual behaviour in rats in two ways, i. e., via its aromatization to oestradiol in the brain, and by stimulating growth of peripheral tissues via its 5α-reduction to dihydrotestosterone. In support for this view we have found that the combination of 19-hydroxytestosterone propionate and dihydrotestosterone propionate was effective in restoring the full pattern of sexual behaviour in castrated male rats.

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