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At least 1,333 records · Page 74Linked to original sources
PubMed1982

Study of the direct action of luteinizing hormone-releasing hormone agonists at the testicular level in intact rats treated with an antiluteinizing hormone serum.

Is it well known that LHRH agonists can inhibit testicular functions by gonadal desensitization secondary to endogenous LH release and that a direct action at the gonadal level has also been demonstrated. Since an excess of anti-LH serum can be used, as an alternative to hypophysectomy, to neutralize the influence of endogenous LH release, the relative importance of the testis and pituitary gland in the inhibitory effect of a LHRH agonist, [D-Ser-(TBU)6,des-Gly-NH210]LHRH ethylamide (Buserelin), was studied on gonadal gonadotropin receptors in intact adult male rats treated with equine anti-LH or normal horse serum (NHS). A single administration of increasing doses (1-100 ng) of Buserelin leads to a progressive inhibition of testicular LH and PRL receptor levels by 70% and 40%, respectively, in animals injected with NHS. Treatment with the anti-LH serum completely prevents this inhibitory effect of a single dose of the LHRH agonist. After two successive injections of Buserelin in NHS-treated animals, testicular LH receptors are reduced by 70% and 80% with the 100- and 500-ng doses, respectively, while testicular PRL receptors are inhibited by 40-60%. In animals treated with the anti-LH serum, the inhibition of testicular LH receptors is reduced by only 18% (100 ng Buserelin) and 55% (500 ng Buserelin), while the inhibitory effect on PRL receptors is abolished. The present data show that endogenous LH release induced by a single injection of a LHRH agonist plays an essential role in the loss of testicular LH receptors measured 2 days later. Moreover, upon repeated injection of the LHRH agonist, neutralization of endogenous LH release by an anti-LH serum markedly reduces the inhibitory effect of the LHRH agonist on LH receptors, while it completely prevents the effect on PRL receptors, suggesting that the inhibitory effect of the LHRH agonist in the male rat is predominantly due to endogenous LH release rather than to a direct action of the peptide at the testicular level.

Animals↗
PubMed1982

Discriminative effects of testosterone on hypothalamic luteinizing hormone-releasing hormone levels and luteinizing hormone secretion in castrated male rats: analyses of dose and duration characteristics.

We have previously reported that in castrated male rats gonadal steroids can raise LHRH levels in the medial basal hypothalamus (MBH). However, there was an important dissociation between episodic LH release and the MBH LHRH response to 17 beta-estradiol. In the present study we have examined the effects of varying the dose of testosterone (T) on the MBH LHRH levels, episodic LH release pattern, and pituitary responsiveness to LHRH; in addition we have determined the duration of T exposure required to elicit the MBH LHRH response. Results show that low serum levels of T (413-638 pg/ml) were just as effective as higher concentrations (1337-1776 pg/ml) in raising the MBH LHRH levels at 96 h; the minimum duration of exposure to T was 72 h. However, whereas higher T levels (greater than 1 ng/ml) suppressed LH release coincident with elevated LHRH levels, low T concentrations did not alter LH release contemporaneous with the MBH LHRH elevations. Analysis of the episodic LH secretion pattern disclosed that these low concentrations of T changed neither the number of pulses per 3 h per rat, pulse amplitude, nor the interpulse interval. On the other hand, as T concentrations were increased, pulse amplitude fell in a dose-related manner while other components of episodic LH secretion remained unchanged. Despite these differential effects of T on the LH release pattern, pituitary sensitivity to exogenous LHRH was reduced by the low as well as high levels of T. These studies show that 1) T can activate those intracellular neurosecretory events that are involved in augmented LHRH supply to the nerve terminals in the median eminence; 2) T can stimulate LHRH accumulation in the MBH by mechanisms that may not involve inhibition of LHRH release; and 3) higher T levels do not alter LH pulse frequency but depress only the pulse amplitude that may result from decrements in the amounts of LHRH released with each neural episode and depressed pituitary sensitivity to LHRH.

Animals↗
PubMed1983

The luteinizing hormone-releasing hormone (LHRH)-desensitized rat pituitary: luteinizing hormone responsiveness to LHRH in vitro.

Desensitization of the anterior pituitary has been observed after continuous infusion of LHRH or repetitive administration of LHRH at concentrations or frequencies exceeding physiological limits. We have studied the LH responsiveness of the LHRH-desensitized male rat anterior pituitary in a continuously perifused dispersed cell culture system. Infusion of 10 nM LHRH initially stimulated a 4- to 5-fold increase in LH secretion which became maximal at 6-9 min and which declined gradually to a preinfusion baseline over 6 h. Since the cells did not maintain peak levels of LH secretion in the presence of continuous exposure to LHRH, they were considered to be desensitized. These desensitized cells were studied to determine their LH responsiveness to LHRH. Cells desensitized by a 6-h LHRH infusion responded to four hourly LHRH boluses of 200 pm by releasing four statistically equal LH pulses. The response of desensitized cells to 200 pm LHRH was similar to that of 10 pm LHRH of nondesensitized cells. Furthermore, desensitized anterior pituitary cells responded to LHRH in a linear dose-dependent manner. The dose response of desensitized cells ranged from 75-500 pm, whereas for nondesensitized cells a dose response was observed from 1-75 pm. In addition, anterior pituitary cells desensitized with continuous LHRH infusion can respond to a second LHRH infusion of a greater concentration and become desensitized for a second time. These data suggest that the capacity of the pituitary gland to store and secrete LH while desensitized is similar to that of the nondesensitized anterior pituitary. The major difference between cells desensitized with LHRH and nondesensitized cells is that desensitized cells require a larger dose of LHRH to elicit a given LH response.

Animals↗
PubMed1983

Prolactin suppresses luteinizing hormone secretion and pituitary responsiveness to luteinizing hormone-releasing hormone by a direct action at the anterior pituitary.

In pathological or experimental hyperprolactinemia, the elevated circulating levels of PRL are the usual cause of the impairment in gonadotropic function. The present study was undertaken to determine whether PRL could suppress basal LH secretion and LHRH-stimulated LH release by a direct action at the anterior pituitary. Anterior pituitaries from ovariectomized rats were incubated in medium 199 alone or in medium 199 containing ovine PRL, and basal and the LHRH-stimulated LH release were followed for 2 or 3 h in vitro. Ovine PRL at 40 and 80 micrograms/ml suppressed basal LH release by 41% and 72%, respectively, at 2 h of incubation. This suppressive effect of both concentrations of PRL continued to the third hour of incubation. LHRH at 5 ng/ml increased the release of LH from pituitaries incubated in medium alone by 57%, 61%, and 107% at 1, 2, and 3 h of incubation, respectively. However, in the pituitaries treated with 40 micrograms/ml ovine PRL, the stimulatory effects of LHRH were diminished at all time points measured. Pretreatment of anterior pituitaries with ovine PRL for 6 h significantly inhibited by 81% the LHRH (5 ng/ml) stimulation of LH release at 2 h of incubation. On the other hand, inhibition of endogenous PRL release by 10(-6) M bromocriptine enhanced the stimulatory effects of 5 ng/ml LHRH by 2.5-fold at 2 h of incubation. The inhibitory effects of PRL on basal and stimulated LH secretion appeared unique, since neither BSA nor vasopressin could elicit similar suppressive effects on LH. These results suggest that in anterior pituitaries exposed to elevated levels of PRL, LH secretion and pituitary responsiveness to LHRH could be impaired. This phenomenon may contribute in part to the antigonadotropic effects of PRL.

Animals↗
PubMed1983

Is the postovulatory release of follicle-stimulating hormone in the rabbit mediated by luteinizing hormone-releasing hormone?

Studies were performed to determine whether the postovulatory secretion of FSH in the rabbit is an LHRH-mediated event. Does were mated and then injected at 12 and 18 h postcoitum with pentobarbital (30 mg/kg BW), an agent known to block endogenous LHRH release. The injection of this barbiturate had no measurable effect on the postovulatory FSH secretion pattern. Administration of the LHRH antagonist [Ac-D-p-C1-Phe1,2, Phe3, D-Arg6, D-Ala10]LHRH (0.5 mg/doe) prevented all gonadotropin release in response to LHRH injection (10 micrograms/kg BW). When this same dose of the antagonist was injected at 18 h postcoitum, the postovulatory FSH secretion pattern was unaffected. Finally, to prove that the pituitary was sensitive to LHRH at 18-h postcoitum, LHRH (10 micrograms/kg BW) was injected into rabbits mated 18 h earlier; this treatment led to a marked increase in FSH secretion showing that the pituitary is responsive to LHRH at this time. The results of this study show that two drugs which block LHRH-mediated gonadotropin release have no effect on the postovulatory secretion of FSH and support the concept that this episode of FSH secretion occurs via a pathway which does not include the hypothalamic secretion of LHRH.

Animals↗
PubMed1983

Synthesis, luteinizing hormone-releasing activity, and receptor binding of chicken hypothalamic luteinizing hormone-releasing hormone.

Chicken hypothalamic LHRH, which was recently structurally characterized, was synthesized by solid-phase methodology, characterized, and tested for LH-releasing activity using anterior pituitary cells from chickens and sheep, as well as for binding to chicken and rat anterior pituitary membrane receptors. Synthetic chicken LHRH exhibited identical properties to the isolated natural chicken LHRH in several chromatographic systems. Synthetic chicken LHRH displayed identical activity to natural chicken LHRH in stimulating LH release from dispersed chicken anterior pituitary cells, and synthetic mammalian LHRH was equipotent in this system. Both the natural and synthetic chicken peptides had similar low potency in stimulating LH release from cultured ovine anterior pituitary cells (approximately 1% of the potency of synthetic mammalian LHRH). The ED50 of binding to rat anterior pituitary membrane receptors was 2.5 X 10(-6) M for synthetic chicken LHRH, compared to 6.3 X 10(-8) M for synthetic mammalian LHRH.

Animals↗
PubMed1984

Developmental changes in luteinizing hormone secretion in the female guinea pig. I. Effects of ovariectomy, estrogen, and luteinizing hormone-releasing hormone.

Negative feedback regulation of LH release was studied by ovariectomy and estrogen treatment in female guinea pigs of four different ages (days 10, 30, 50, and 150). The average age at first ovulation in guinea pigs in our colony was 60.1 +/- 2.2 days (n = 33). Bilateral ovariectomy (OVX) on day 30, 50, or 150 of age resulted in a sharp increase in serum LH concentrations within 3 days, and this rise continued for 9 days, when LH values reached a plateau. In contrast, when OVX was performed on day 10 of age, only a slight elevation in LH levels was observed during the first 16 days after surgery. Twenty days after OVX (day 30 of age), LH concentrations started to increase rapidly and reached the maximum value on day 38 of age; this latter response was similar to that observed immediately after OVX in animals in the three older age groups. Serum LH concentrations after LHRH administration (2 micrograms/kg BW) were similar in ovariectomized females on days 23 and 43 of age, suggesting that the postcastration increase in LH secretion after day 26 of age was not due to a change in pituitary sensitivity. Daily injections of estradiol benzoate at doses of 0.5 and 2.0 micrograms/kg BW from 15-20 days after OVX suppressed LH levels in all four age groups. The present findings indicate that an increase in the capacity for LH release occurs around day 30 in the female guinea pig. Since this increased LH release is not due to an apparent change in pituitary sensitivity to LHRH, the endogenous release of LHRH may be inhibited before day 30 of age. These results suggest that an alteration in the regulation of LH release by the brain may occur before the onset of puberty in female guinea pigs.

Aging↗
PubMed1990

Interleukin-1 inhibits the ovarian steroid-induced luteinizing hormone surge and release of hypothalamic luteinizing hormone-releasing hormone in rats.

Interleukin-1 (IL-1), a polypeptide cytokine secreted by activated macrophages, has been postulated as a chemical messenger between the immune and endocrine systems. IL-1-immunopositive neurons and fibers have been visualized in the human and rat hypothalamus, and IL-1 receptors are present in the rat brain. We have examined the effects of human recombinant IL-1 (alpha- and beta-subtypes) on LH release in vivo and hypothalamic LHRH release in vitro. Ovariectomized rats were primed with estradiol benzoate, and progesterone was injected 48 h later to elicit a LH surge in the afternoon. IL-1 alpha and IL-1 beta were injected either intracerebroventricularly (icv) via a preimplanted cannula in the third ventricle of the brain or iv. Systemic injection of IL-1 alpha or IL-1 beta (58.8 pmol at 1300 and 1500 h) failed to influence the afternoon LH surge seen in saline-injected control rats. However, IL-1 beta (1.76 pmol) administered icv at 1300 and 1500 h or a single icv injection at 1300 h blocked the progesterone-induced LH surge. Similar icv injections of IL-1 alpha also significantly suppressed the afternoon LH surge compared to that in saline-injected control rats. However, IL-1 alpha was relatively less effective than the beta-subtype, since the LH surge was detected in some rats. To ascertain whether suppression of the LH surge was due to inhibition of LHRH release, the medial basal hypothalamus-preoptic area of estradiol benzoate-progesterone-treated ovariectomized rats was incubated with and without IL-1. Both IL-1 alpha and IL-1 beta, at concentrations of 0.1 nM and higher, significantly suppressed LHRH release in vitro from the medial basal hypothalamus-preoptic area. In contrast, IL-1 (10 nM) was completely ineffective in suppressing LHRH release from the microdissected median eminence. These results demonstrated an overall inhibitory effect of icv IL-1 on the LHRH-LH axis and suggest that suppression of the steroid-induced LH surge by IL-1 may primarily be due to inhibition of LHRH release at hypothalamic sites located within the blood-brain barrier.

Animals↗
PubMed1990

Progesterone enhances the surge of luteinizing hormone by increasing the activation of luteinizing hormone-releasing hormone neurons.

The ability of progesterone (P) to enhance the surge of LH in the rat is well documented, but whether its primary site of action is on the pituitary or brain is unclear. To determine whether P can alter the activation of LHRH neurons, 1) intact female rats were treated with the P antagonist RU486 (5 mg) at 1230 h on proestrus and killed at specified times during the afternoon and evening for comparison of plasma LH levels and cFos expression in LHRH neurons with untreated proestrous rats. RU486 treatment greatly reduced both the magnitude of the LH surge and the degree of cFos induction (numbers of cells expressing cFos and intensity of cFos staining) in LHRH neurons during proestrus. 2) Ovariectomized (OVX) rats were primed with estradiol benzoate (EB, 1 microgram) and then were treated with EB alone (50 microgram) or EB plus P (5 mg). Treatment with EB without P resulted in significantly lower peak LH levels and a reduced cFos response in LHRH neurons than the EB-P treated rats. These data suggest that the actions of P eventuate in an enhanced activation of LHRH neurons that may be responsible for the increased magnitude of the LH surge.

Animals↗
PubMed1976

Reduced luteinizing hormone release by synthetic luteinizing hormone-releasing hormone (LHRH) in postpartum lactating rats.

The ability of the pituitary to release LH in response to synthetic LHRH was tested in lactating female rats on days 7 and 17 post partum, and compared with that of normal cycling female rats on diestrous day 2 (controls). Three consecutive injections of LHRH (100 ng/100 g BW, sc), each 50 min apart, were given to each rat and sequential blood samples were collected at 25-min intervals by cardiac puncture under light ether anesthesia. In all 3 groups, the 2nd and 3rd injections of LHRH produced much greater increases in serum concentrations of LH than the 1st injection. However, this self-priming effect of LHRH on LH response was markedly attenuated in the postpartum lactating rats (PPL), compared with the normal cycling female rats on diestrous day 2. Three consecutive injections of LHRH produced significantly less LH release in PPL rats than in normal cycling female rats on diestrous day 2. Both day 7 and day 17 PPL rats released equally small amounts of LH in response to LHRH administration. The total amount of LH released by anterior pituitaries (APs) during a 5 h incubation in medium-199, from day 7 or day 17 in PPL rats, was significantly less than that released by the APs from normal cycling female rats on diestrous day 2. APs from day 7 and day 17 PPL rats also released less LH in vitro in response to LHRH (50 ng) stimulation than APs from normal cycling female rats. When APs from normal cycling female rats on diestrous day 2 were incubated with LHRH, the increments in LH release were greater at the end of the 2nd and 3rd h than after the 1st h of incubation. However, such increments in LH release were relatively small when APs from day 7 or day 17 PPL rats were similarly incubated with LHRH.

Animals↗
PubMed1996

Use of newly designed microperifusion system with amperometric sensors for near-continuous on-line monitoring of hormone secretion. I. correlation with the luteinizing hormone secretory response to gonadotropin-releasing hormone.

LH is rapidly secreted from the anterior pituitary gland in response to episodic release of GnRH. To understand better the detailed dynamics of this secretory process and related time- and dose-dependent effects, we developed a microperifusion system able to preserve resolution of dynamic secretory responses by minimizing dispersion and with capabilities for automation and continuous on-line monitoring. To monitor secretion at a frequency greater than that feasible with discrete samples, we determined whether LH or another molecule cosecreted by anterior pituitary cells could be monitored on a near-continuous basis using amperometric electrochemical sensors operated under conditions of cyclic voltammetry. The developed culture system incorporated a 32-mu l cell chamber in a controllable constant environment. Miniature sensors were positioned immediately adjacent to the cells to permit differential measurements of the input and effluent streams of medium. With the system, square wave pulses of electrochemically active, biologically inert molecules, e.g. ascorbate and phenol red, showed similar redox profiles before and after the cells, with minimal dispersion. Enzymatically dispersed ovine anterior pituitary cells were cultured on SoloHill glass beads for 4 days, loaded into the chamber, and perifused with DMEM containing 10% FCS for 2 h. After stabilization, the medium was switched to protein-free, HEPES-buffered HBSS with L-glutamine and allowed to flow for a 1-h washout period, followed by GnRH challenges of varying concentrations in a random order. Perifusate was collected in six-drop fractions at approximately 30-sec intervals. Although LH, its individual subunits, and FSH could not be detected amperometrically, GnRH stimulation of the cells simultaneously induced a several log order dose-dependent secretion of both an electrochemically detectable molecule and LH, as measured by RIA. The secretory profiles of the amperometrically detected signal and immunoactive LH were very similar. Dose-response relationships of the amperometric signal and LH to a wide range of GnRH were similar. The responses of both secreted LH and the amperometric signaling molecule(s) to GnRH were triphasic; an initial peak of activity was observed within 20-40 sec, a lower plateau level was observed for the duration of the 4-min GnRH stimulation, and a gradual return to baseline followed. The cells then maintained a constant level of GnRH-independent basal secretion. These results indicate that it is feasible to monitor the complex dynamics of endocrine and cellular responsiveness to secretagogues from endocrine cells/tissues continuously in real-time.

Animals↗
PubMed2005

Treatment with growth hormone and luteinizing hormone releasing hormone analog improves final adult height in children with congenital adrenal hyperplasia.

Final adult height is often compromised in children with congenital adrenal hyperplasia (CAH). This study examines the impact of GH and LHRH analog (LHRHa) on final adult height in patients with CAH due to 21-hydroxylase deficiency. Fourteen patients with CAH (eight males, six females) predicted to be more than 1.0 sd below their midparental target height received GH and LHRHa until final height. Each patient was matched at the start of GH therapy to a CAH patient treated only with glucocorticoids according to type of CAH, sex, and chronological age. Mean age, bone age, height, height prediction, and target height were the same in both groups at the beginning of GH therapy. Mean duration of GH treatment was 4.4 +/- 1.5 yr. Mean duration of LHRHa therapy was 4.2 +/- 2.0 yr. In the treatment group, final height sd score of -0.4 + 0.8 was significantly greater than both the initial prediction of -1.5 +/- 0.9 (P < 0.0001) and the final height sd score of the untreated group of -1.4 +/- 1.1 (P = 0.01). Our results indicate that the combination of GH and LHRHa improves final adult height in patients with CAH.

Adolescent↗
PubMed1978

Induction of growth hormone and prolactin secretion by luteinizing hormone-releasing hormone and its blockade by bromoergocriptine in acromegalic patients.

In an attempt to evaluate the effect of LRH on GH and PRL secretion, LRH in a dose of 100 micrograms was injected iv to 22 patients with active acromegaly. A definite increase in both serum GH and PRL levels was observed in one patient, while four other subjects responded to LRH to secret either GH or PRL. The effectiveness of LRH on GH and PRL release was not correlated with the age or sex of patients, the basal levels of serum GH or PRL, the GH response to TRH administration, or the increase in serum gonadotropin concentrations after LRH injection. In three patients, this LRH-induced GH and PRL release was completely blocked by pretreatment with 2-bromo-alpha-ergocriptine (CB154). The results suggest that elevations of GH and PRL after LRH occur rather sporadically in acromegalic patients and that the action of LRH on GH release is occasioned by a different mechanism from that of TRH.

Acromegaly↗
PubMed1979

Plasma cortisol response to thyrotropin-releasing hormone and luteinizing hormone-releasing hormone in Cushing's disease.

In 3 of 6 patients with pituitary-dependent Cushing's disease, a paradoxical increase of plasma cortisol was observed both after LRH (delta max, 13.9 +/- 3.7 microgram/100 ml; 113 +/- 52%) and TRH (delta max, 8.0 +/- 2.9 microgram/100 ml; 53 +/- 18%) administration, the maximum values being achieved 30--60 min after the iv bolus injection. In the remaining 3 patients and in 15 control subjects, plasma cortisol levels did not rise in response to either LRH or TRH administration but rather showed a slight to distinct decrease during the study period. The paradoxical cortisol response in half of the patients with Cushing's disease may be the consequence of loss of specificity of the pituitary receptor or alteration in the hypothalamo-pituitary pathways.

Adult↗