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PubMed1983

Clomiphene citrate induces luteinizing hormone release through hypothalamic luteinizing hormone-releasing hormone in vitro.

The releasing effects of clomiphene citrate (clomiphene) on luteinizing hormone (LH) and LH-releasing hormone (LRH) were examined in a sequential double chamber superfusion system by superfusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normal female rats in dioestrus. When the MBH and the pituitary were superfused in sequence with medium containing 2 X 10(-10) M oestradiol (E2), two significant peaks in LH release (60-130% increase, P less than 0.05) were observed 40 min and 90 min after the administration of 3 X 10(-8) mol clomiphene. Administration of clomiphene in medium without E2 induced a low peak (25-50% increase, P less than 0.05) of LH released from the pituitary perfused in series with the MBH. Administration of clomiphene did not cause a marked increase of LH from the pituitary superfused alone, when superfused with or without E2 containing medium. The concentration of LRH in the efflux was significantly increased (50-100%) 40 min and 90 min after clomiphene administration when MBH was superfused with medium containing E2, whereas clomiphene had no effect when superfused with medium alone. These data indicate: 1) that clomiphene induces LRH release from the MBH, that it may induce LH release, in part, by acting directly at the pituitary level; 2) that changes in LH after clomiphene administration coincide with LRH release, and 3) that a certain concentration of E2 may be necessary for the secretion of LRH by clomiphene.

Animals↗
PubMed1983

Relationships between serum prolactin levels and follicle stimulating hormone response to luteinizing hormone-releasing hormone during early puerperium.

The effect of serum prolactin (Prl) levels on pituitary response to iv luteinizing hormone-releasing hormone (LRH) (100 micrograms) was studied in 23 normal puerperal women on day 1 post-partum. All women had an uneventful full-term pregnancy and delivery. The LRH test was repeated in 8 of the women on day 3 and in the remaining 15 on day 6 post-partum. Serum Prl levels were high on days 1 and 3, but decreased significantly on day 6 (P less than 0.01). No pituitary FSH response to LRH stimulus was found on day 1 post-partum in all 23 women. In those who were given placebo, FSH levels in serum did not change in response to LRH on day 3 (4 women), but increased significantly on day 6 (5 women) in all subjects (P less than 0.05). Conversely, when oral metoclopramide was given from day 1 to 6 (10 women) the responsiveness of FSH to LRH on day 6, found in the placebo group, was not observed. Early reduction of serum Prl values on day 3 post-partum by bromocriptine treatment from day 1 to 3 (4 women) did not accelerate the FSH response to LRH. These results suggest an inhibitory effect of elevated serum Prl on the pituitary FSH response to LRH in women during early puerperium.

Adult↗
PubMed1975

Identification of human luteinizing hormone, follicle-stimulating hormone, luteinizing hormone beta-subunit and gonadotrophin alpha-subunit in foetal and adult pituitary glands.

Specific radioimmunoassays were used to assess the content of LH, FSH, the gonadotrophin alpha-subunit and the LH beta-subunit in four adult, 19 normal foetal pituitary glands (9-5--32 weeks of gestation) and a pituitary extract from an anencephalic foetus (36 weeks). The hormones and subunits were further identified by column chromatography on Sephadex G-100. All pituitary glands contained free alpha-subunit and intact LH but the alpha-subunit:LH ratio was significantly higher in the early foetal pituitaries (9-5--16 weeks) than in the four adult pituitaries. Only small or undetectable amounts of LH beta-subunit and 'undetectable' FSH were found in these early foetal pituitaries (9-5--11-5 weeks). The concentration of intact hormones or subunits in the pituitaries showed no significant sex difference in any of the groups. In contrast to these results, only alpha-subunit was detectable in the pituitary of the anencephalic foetus. For 14 early foetuses (age of gestation 10--16 weeks) the serum levels of LH-HCG, FSH, and alpha-subunit in the circulation were significantly higher than in 26 foetuses at term (37--41 weeks). On the basis of these results a theory for the development of the gonadotrophin secretion from the foetal pituitary gland is outlined.

Adult↗
PubMed1976

Application of an in-vitro perifusion technique to studies of luteinizing hormone release by rat anterior hemi-pituitaries: Self-potentiation by luteinizing hormone releasing hormone.

A technique is described for the continuous perifusion of rat adenophypophyses. Exposure of the perifused glands to repeated equal 5 min stimuli with hypothalamic extract resulted in a series of equal peaks of corticotrophin secretion, the response was proportional to log dose over the range 0 - 25-2 - 0 rat hypothalamic equivalents/ml. Repeated equal stimuli with hypothalamic extract, or with luteinizing hormone releasing hormone (LH-RH) at concentrations of 2 or 10 ng/ml, resulted in a progressively increasing series of peaks of LH secretion, i.e. a self-potentiating or priming effect. The effect took between 30 min and 1 h to develop. A delayed increase in the responsiveness of the glands was also seen with continuous incubation of anterior pituitaries with LH-RH. The relevance of these observations to the physiological control of LH secretion is discussed.

Adrenocorticotropic Hormone↗
PubMed1976

Secretion of luteinizing hormone caused by continuous infusions of luteinizing hormone releasing hormone in the long-term ovariectomized rat: effect of oestrogen pretreatment.

Continuous infusions of luteinizing hormone releasing hormone (LH-RH) into phenobarbitone-treated long-term ovariectomized rats, resulted in patterns of LH secretion which were determined by the blood LH-RH concentration. Infusions of 52 ng LH-RH/h caused steadily increasing ple maintained for the rest of the experiment (9h). A similar course of plasma LH concentration was observed as a result of infusions of 104 ng LH-RH/h, though in this case LH concentrations reached higher levels than those induced by infusion of 52 ng LH-RH/h. Higher rates of LH-RH infusion (208 and 416 ng/h), however, induced clear-cut LH peaks, which reached their maximal plasma values after 2-3 h of infusion and then declined again until, at the end of the experiment, they were only slightly higher than the LH levels induced by infusions of 52 ng LH-RH/h. A similar series of LH-RH infusions given to ovariectomized rats pretreated with oestradiol benzoate during 3 days (the rats were injected daily with 7 mug steroid), produced a highly augmented response of the pituitary gland, but all LH-RH concentrations infused induced rather sharp LH peaks, reaching their maximum after 2-3 h of infusion. After 5 h of infusion the descending parts of all these peaks appeared to converge. In both control and oestradiol benzoate-pretreated rats there appeared to be a linear relationship between the logarithm of the blood LH-RH concentration and the maximal plasma LH values on one hand, and the amount of LH secreted during the first 5 h of infusion on the other. Furthermore, it appeared that the longer the period of oestrogen action, the more the response of the pituitary gland to a certain dose of LH-RH was enhanced.

Animals↗
PubMed1978

Steroid priming of the luteinizing hormone response to luteinizing hormone releasing hormone.

Perifusion experiments were performed to study the stimulatory effects of luteinizing hormone releasing hormone (LH-RH) on the release of LH from anterior pituitary tissue. Exposure of pituitary tissue from normal male rats to LH-RH (5 ng/ml for 5 min) induced a small release of LH; in tissue from ovariectomized rats receiving no pretreatment, the release was more than three times greater and in tissue from gonadectomized male or female rats pretreated with oestradiol benzoate and progesterone, the release was six times greater than that observed in normal rats. Further exposure of pituitary tissue from gonadectomized steroid-pretreated male and female rats to LH-RH (5 ng/ml) induced an increase in the level of LH even greater than that seen after the initial exposure (priming action of LH-RH); in tissue from ovariectomized rats receiving no pretreatment, less LH was released than after the first exposure to LH-RH and in tissue from normal male rats the response was unchanged.

Animals↗
PubMed1978

Effects of dexamethasone on the responses of luteinizing hormone and testosterone to two injections of luteinizing hormone releasing hormone in young postpubertal bulls.

Six young postpubertal bulls were studied in two experiments, 3 months apart. In experiment 1, three bulls received i.m. injections of dexamethasone (20 mg) and 5 h later these animals plus three control bulls received i.m. injections of luteinizing hormone releasing hormone (LH-RH, 250 microgram). In experiment 2, the controls from experiment 1 received dexamethasone and the treated animals from experiment 1 acted as controls for experiment 2. All bulls also received an i.m. injection of 250 microgram LH-RH on day 2 of each experiment. The concentrations of LH and testosterone in samples of jugular blood were determined by radioimmunoassay. There were no significant differences in the patterns of testosterone and LH release between the two experiments. On day 1, the response of LH to LH-RH was significantly (P less than 0.05) reduced by dexamethasone, but on day 2 values in the control and treated groups were similar although significantly (P less than 0.05) lower than values on day 1. The response of testosterone to LH-RH was not affected by dexamethasone. These results are discussed in terms of the site of action at which dexamethasone may act to depress the release of LH.

Animals↗
PubMed1979

Suppression of the luteinizing hormone releasing effect of luteinizing hormone releasing hormone by arginine-vasotocin.

The concentrations of 17-oxosteroids in the spermatic venous blood of anaesthetized dogs were used as an index of LH release to assess the effects of arginine-vasotocin on the response of the canine pituitary gland to exogenous luteinizing hormone releasing hormone (LH-RH). When injected into the carotid artery, arginine-vasotocin (1.0 microgram/kg body wt) caused no significant alterations in the testicular output of 17-oxosteroids. The administration of LH-RH (5 microgram/kg body wt, a standard dose) into the carotid artery produced typical stimulation of testicular 17-oxosteroid secretion. Administration of arginine-vasotocin (0.01, 0.1 or 1.0 microgram/kg body wt) into the carotid artery 3 h before the administration of a standard dose of LH-RH inhibited the testicular secretion of 17-oxosteroids normally induced by LH-RH. However, pretreatment with arginine-vasotocin (1.0 microgram/kg body wt) did not affect the testicular response to i.v. administration of human chorionic gonadotrophin (5 i.u./kg body wt). These results indicate that in the dog, arginine-vasotocin inhibits the LH-RH-induced release of LH by acting acting directly on the anterior pituitary gland.

17-Ketosteroids↗
PubMed1982

Plasma cortisol response to thyrotrophin releasing hormone and luteinizing hormone releasing hormone in healthy kennel dogs and in dogs with pituitary-dependent hyperadrenocorticism.

The change in the plasma concentration of cortisol after the administration of thyrotrophin releasing hormone (TRH) and LH releasing hormone (LH-RH) was studied in normal dogs and in dogs with pituitary-dependent hyperadrenocorticism (PDH). The normal dogs showed a small but significant increase in the plasma concentration of cortisol 15 min after intravenous injection of TRH and LH-RH. In ten of the dogs with PDH the response to TRH was not significantly different from that in the normal dogs, but in 13 the response was significantly greater. In 15 of the dogs with PDH the response to LH-RH administration was within or below the range of responses in the normal dogs and in only one dogs was the response to LH-RH greater than that in the normal dogs. These findings are discussed in relation to the pathogenesis of PDH.

Adrenal Cortex↗
PubMed1989

Effects of growth hormone-releasing hormone on the secretion of islet hormones and on glucose homeostasis in lean and genetically obese-diabetic (ob/ob) mice and normal rats.

The effect of synthetic human growth hormone-releasing hormone(1-40) (hGHRH-40) on the function of the endocrine pancreas and on glucose homeostasis in lean and genetically obese-diabetic (ob/ob) mice and normal rats has been examined. The addition of 1 mumol hGHRH-40/1 to incubated islets from normal lean mice increased insulin release by 90 and 37% at 5.6 and 16.7 mmol glucose/l respectively. Lower concentrations of hGHRH-40 did not affect insulin release. hGHRH-40 (1 mumol/l) increased pancreatic polypeptide release by 50% at 5.6 mmol glucose/l. A range of concentrations of hGHRH-40 (1 nmol/l-1 mumol/l) reduced glucagon release by 42-73% at 5.6 mmol glucose/l, and by 38-70% at 16.7 mmol glucose/l. Somatostatin release was increased (eightfold) by 1 mumol hGHRH-40/1 at 5.6 mmol glucose/1, but at 1 nmol hGHRH-40/1 somatostatin release was reduced (by greater than 50%). At 16.7 mmol glucose/litre 0.01-1 mumol hGHRH-40/1 increased somatostatin release (three- to fourfold), but 1 nmol hGHRH-40/1 produced a reduction of 50%. In vivo, administration of hGHRH-40 (50 micrograms/kg body weight i.p.) to fasted lean and ob/ob mice did not alter basal plasma concentrations of glucose and insulin, or the glucose and insulin responses to a concomitant i.p. glucose challenge. Intravenous injection of hGHRH-40 (20 micrograms/kg body weight) to anaesthetized rats increased plasma concentrations of insulin in the hepatic portal vein. A lower dose of hGHRH-40 (0.2 micrograms/kg) was ineffective, and neither dose of hGHRH-40 altered plasma glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Annual variations in serum thyroid-stimulating hormone and thyroid hormones and in their responses to thyrotrophin-releasing hormone in the reindeer.

The reindeer in its natural habitat is subject to great annual variations in ambient temperature, illumination and nutrition. To ascertain the effect of these environmental factors on thyroid function, serum thyroid-stimulating hormone (TSH), thyroxine (T4), tri-iodothyronine (T3) and reverse T3 (rT3) concentrations were measured four times a year (2 June, 8 October, 21 November, and 24 February) in 14 animals housed outdoors at latitude 69 degrees 10'N. They all showed statistically significant (P < 0.05) seasonal changes. Serum TSH and T4 were highest in February (623 +/- 30 ng/ml and 287 +/- 19 nmol/l respectively). TSH was lowest in October (318 +/- 47 ng/ml) and T4 in November (199 +/- 19 nmol/l). The T3 concentration was highest in November (3.0 +/- 0.3 nmol/l) and lowest in June (1.8 +/- 0.2 nmol/l). In contrast, rT3 was highest in June (3.6 +/- 1.2 nmol/l) and lowest in November (1.9 +/- 0.6 nmol/l). Thus, there was an inverse relationship between T3 and rT3 (linear regression r = -0.406, P < 0.01). TSH, T4, T3 and rT3 responses to exogenous thyrotrophin-releasing hormone (synthetic TRH; 500 micrograms i.m.) were determined in ten animals. The magnitude of their response to TRH was significantly (P < 0.05) dependent on the time of year. When compared with the control level all the parameters rose significantly (P < 0.05). The greatest rise in serum TSH occurred in October (219 +/- 151%) and the smallest in February (66 +/- 53%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Nutritional Physiological Phenomena↗
PubMed1986

Effects of restriction of dietary energy intake during the prepubertal period on secretion of luteinizing hormone and responsiveness of the pituitary to luteinizing hormone-releasing hormone in heifers.

The working hypothesis that a low plane of nutrition during the prepubertal period delays puberty in heifers by retarding the prepubertal increase in secretion of luteinizing hormone (LH) was investigated. Secretion of LH and the responsiveness of the pituitary to LH-releasing hormone (LHRH) were compared in heifers fed a growing diet (which allowed spontaneous occurrence of puberty; n = 12; control) or an energy deficient diet (which delayed puberty; n = 11; delayed) during the prepubertal period. The dietary treatments were initiated when the heifers were 299 +/- 14 (mean +/- SD) d of age (d 0 of the experiment) and continued until d 175 of the experiment (474 +/- 14 d of age). Weight gains were .79 +/- .05 (mean +/- SE) and .21 +/- .03 kg X head-1 X d-1 for control and delayed heifers, respectively. Puberty occurred on d 120 +/- 14 of the experiment (428 +/- 13 d of age) in control heifers, whereas none of the delayed heifers attained puberty during the feeding period. Serum concentration of LH and the frequency of LH pulses increased rapidly during the 175-d feeding period in control heifers. In delayed heifers, serum LH concentration increased less rapidly and no increase in pulse frequency was detected during the experimental period. Amplitude of LH pulses tended to be higher in control than delayed heifers. Responsiveness of LH secretion to LHRH was lower in delayed than control heifers. It is speculated that failure of secretion of LH to increase is the causative factor for delayed puberty when dietary energy is limited during the prepubertal period in heifers.

Animals↗
PubMed1983

Luteinizing hormone release and androgen production of avian hybrids in response to luteinizing hormone releasing hormone injection.

The levels of luteinizing hormone (LH) and androgens were measured in sterile avian hybrids. Guinea fowl-chicken and peafowl-guinea fowl hybrids were bled before and after injection with LH- releasing hormone (LHRH). The preinjection LH levels for the guinea fowl-chicken hybrids were below or at the very lower limit of the assay sensitivity and the peafowl-guinea fowl hybrids averaged 1.3 ng/ml. Within 10 min after LHRH injection, LH had increased dramatically in both hybrids and then began to slowly decline. Androgen levels in the guinea fowl-chicken hybrids increased from 16.2 pg/ml to 95.2 pg/ml and continued to increase, reaching 287 pg/ml at the last bleeding 60 min after injection.

Androgens↗
PubMed1994

[Cloning and characterization of the human thyrotropin-releasing hormone receptor: regulation of thyrotropin-releasing hormone receptor mRNA levels by thyroid hormone].

1) We successfully cloned a human thyrotropin-releasing hormone receptor (TRH-R) gene. The human TRH-R consists of 398 amino acids and is a member of the G protein-coupled receptor family. The gene has a single intron in the coding sequence. Although highly homologous to the rat and mouse TRH-Rs, the human TRH-R has several differences in the carboxyl-terminal structure. 2) We next studied the effect of thyroid status on TRH-R mRNA levels both in vivo and in vitro. TRH-R mRNA levels in hypothyroid rats were increased significantly, while no significant changes were observed in vitro. The data indicate that thyroid hormone may regulate TRH-R mRNA levels in different manners in vitro and in vivo.

Amino Acid Sequence↗
PubMed1982

Gonadotrophin releasing hormone causes a biphasic secretion of luteinizing hormone and follicle stimulating hormone by cultures of rat anterior pituitary cells.

Primary monolayer cultures of adult male rat anterior pituitary cells secreted both LH and FSH in a biphasic manner when incubated with gonadotrophin releasing hormone (GnRH). The peaks of secretion of LH and FSH were coincident: the first occurred between 15 and 30 min and the second between 1 and 3 h after the addition of GnRH. Approximately 20% of the total amount of gonadotrophins secreted in the 6 h treatment with GnRH was contained in the first peak. Inhibitors of the secretion of gonadotrophins affected LH and FSH secretion differently. Inhibin suppressed the secretion of FSH to a greater extent than that of LH, whereas testosterone and cycloheximide had a greater effect on LH. Neither phase of secretion of LH or FSH was reduced preferentially by inhibin or testosterone but the greater effect of cycloheximide was on the second phase of secretion.

Animals↗
PubMed2001

Melanin-concentrating hormone stimulates the release of luteinizing hormone-releasing hormone and gonadotropins in the female rat acting at both median eminence and pituitary levels.

The purpose of this study was to investigate whether melanin-concentrating hormone (MCH) acts directly on the median eminence and on the anterior pituitary of female rats regulating LHRH and gonadotropin release. In addition, immunohistochemistry was used to examine the density and distribution of MCH-immunoreactive fibers in the median eminence of proestrous rats. MCH-immunoreactive fibers were found in both the internal and external layers of the median eminence and in close association with hypophysial portal vessels. In the first series of in vitro experiments, median eminences and anterior pituitaries were incubated in Krebs-Ringer bicarbonate buffer containing two MCH concentrations (10(-10) and 10(-8) M). The lowest MCH concentration (10(-10) M) increased (P < 0.01) LHRH release only from proestrous median eminences. Anterior pituitaries incubated with both MCH concentrations also showed that 10(-10) M MCH increased gonadotropin release only from proestrous pituitaries. In the second series of experiments, median eminences and pituitaries from proestrous rats were incubated with graded concentrations of MCH. MCH (10(-10) and 10(-9) M) increased (P < 0.01) LHRH release from the median eminence, and only 10(-10) M MCH increased (P < 0.01) LH and FSH release from the anterior pituitary. The effect of MCH on the stimulation of both gonadotropins from proestrous pituitaries was similar to the effect produced by LHRH. Simultaneous incubation of pituitaries with MCH and LHRH did not modify LH but increased the FSH release induced by LHRH. The present results suggest that MCH could be involved in the regulation of preovulatory gonadotropin secretion.

Animals↗
PubMed1996

Chronic administration of a new potent agonist of growth hormone- releasing hormone induces compensatory linear growth in growth hormone-deficient rats: mechanism of action.

To assess the efficacy of a potent agonist analog of GH-releasing hormone (GH-RH), [Dat1,Gln8,Orn12,21,Abu15,Nle27,Asp28,A gm29]hGH-RH(1-29) (JI-38), we investigated the effects of its chronic administration on growth responses in monosodium glutamate (MSG)-lesioned and normal young rats. Body weight (BW), body length (BL), tibia length (TIL), and tail length (TAL) were monitored. Basal serum GH concentrations, GH responses to bolus injections of GH-RH, pituitary GH and serum IGF-I concentrations were measured by RIA. Pituitary GH-RH receptor concentration and binding affinity was also evaluated after the treatment. Neonatal treatment with MSG resulted, as expected, in blunted growth and a decrease in serum and pituitary GH concentration and serum IGF-I levels. A reduction in GH-RH receptor concentration, associated with increased binding affinity of the GH-RH receptor was also found. Chronic administration of GH-RH agonist JI-38 in doses of 2 micrograms at 12-hour intervals for 2 weeks markedly increased the GH responsiveness to GH-RH and stimulated growth, with MSG-treated animals achieving the growth rate of normal controls. Acceleration of growth was associated with stimulated GH synthesis and IGF-I secretion, although basal serum GH levels did not change. Pituitary GH-RH receptor concentration and binding affinity were not significantly modified by the treatment. Treatment of normal young growing rats with agonist JI-38 did not further increase the normal growth acceleration in these rats, but stimulated the GH synthesis and augmented the GH secretory responsiveness. The treatment of MSG-lesioned rats with GH-RH agonist was generally more effective in female than in male animals, and in some cases masked the sex differences in growth rate. Our findings provide the first evidence that the blunted growth rate of the MSG-lesioned rats is associated with a decreased pituitary GH-RH receptor concentration. Our work demonstrates that administration of GH-RH agonist JI-38 is able to restore the normal growth rate of the GH-deficient rats by stimulating GH synthesis and IGF-I secretion.

Animals↗