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At least 415 records · Page 23Linked to original sources
PubMed1988

Are fetal adrenocorticotropic hormone and renin secretion suppressed by maternal cortisol secretion?

Previous studies from this laboratory have demonstrated that intravenous infusions of hydrocortisone (cortisol) into fetal sheep at rates that produce plasma concentrations achieved during fetal stress inhibit fetal adrenocorticotropic hormone (ACTH) and renin secretion. The present study was designed to test for inhibition of fetal renin and ACTH after maternal adrenal secretion of cortisol. ACTH-(1-24) or saline infusion into 12 pregnant ewes (120-132 days gestation) at rates of 0, 1, 5, or 20 ng ACTH.kg-1.min-1 for 5 h produced dose-related increases in maternal plasma ACTH and cortisol concentrations and fetal plasma cortisol concentration. In the 20-ng.kg-1.min-1 group, increases in fetal plasma cortisol of 8.0 ng/ml (to 24.3 +/- 3.7 ng/ml) did not suppress basal fetal plasma renin activity. One hour after the end of the maternal vehicle or ACTH infusion, fetal ACTH secretion was stimulated by fetal intravenous infusion of sodium nitroprusside. In the 0-, 1-, and 5-ng.kg-1.min-1 groups, fetal ACTH responses to nitroprusside were suppressed in animals infused with ACTH. Together, these results indicate that the maternal adrenal secretion of cortisol inhibits stimulated secretion of ACTH but not renin in 120- to 132-day-gestation fetal sheep.

Adrenocorticotropic Hormone↗
PubMed1997

Effect of glandular kallikrein on distal nephron HCO3- secretion in rats and on HCO3- secretion in MDCK cells.

Renal kallikrein is localized in the connecting tubule cells and secreted into the tubular fluid at late distal nephron segments. The present experiments were performed to further test the hypothesis that renal kallikrein reduces bicarbonate secretion of cortical collecting duct (CCD). The effect of orthograde injections of pig pancreatic kallikrein (1 or 3 micrograms/ml) into the renal tubular system was investigated. Urine fractions (Fr) were collected after a 2-min stop flow. Changes in the urine fraction with respect to those in free-flow urine samples (Ff) were related to the respective polyfructosan (Inutest) ratio. Renal kallikrein activity (Fr:Ff kallikrein/ Fr:Ff polyfructosan) increased significantly in the first two urine fractions collected after glandular kallikrein administration (kallikrein, 1 microgram/ml, P < 0.05; kallikrein, 3 micrograms/ml, P < 0.01). HCO3- secretion of collecting ducts was significantly reduced dose dependently by orthograde and also reduced by retrograde pig pancreatic kallikrein administration. Release of kinins into the fractions was not affected by the retrograde kallikrein injection, even though the kallikrein activity increased considerably (2.26 +/- 0.2 vs. 1.55 +/- 0.2, P < 0.05). Adequacy of retrograde injections for delivering substances to the CCD was demonstrated by injecting colloidal mercury and detecting the appearance of this mercury in the renal cortex by transmission electron microscopy. The integrity of the renal tissue after a retrograde ureteral injection was confirmed by scanning electron microscopy. These results confirm and extend previous data (M. Marin-Grez and P. Vallés. Renal Physiol. Biochem. 17: 301-306, 1994; and M. Marin-Grez, P. Vallés, and P. Odigie. J. Physiol. 488: 163-170, 1995) showing that renal kallikrein reduces bicarbonate secretion at the CCD, probably by inhibiting HCO3- transported by a mechanism unrelated to its kininogenase activity. Support for this assessment was obtained in experiments testing the effect of kallikrein on the luminal bicarbonate secretion of a subpopulation of Madin-Darby canine kidney cells capable of extruding the anion. Kallikrein inhibited HCO3-/Cl- exchange, and the degree of inhibition was dose dependent. This inhibition occurred in the absence of kininogen in the bathing solution.

Animals↗
PubMed2005

Selective identification of secreted and transmembrane breast cancer markers using Escherichia coli ampicillin secretion trap.

Secreted and cell surface proteins play important roles in cancer and are potential drug targets and tumor markers. Here, we describe a large-scale analysis of the genes encoding secreted and cell surface proteins in breast cancer. To identify these genes, we developed a novel signal sequence trap method called Escherichia coli ampicillin secretion trap (CAST). For CAST, we constructed a plasmid in which the signal sequence of beta-lactamase was deleted such that it does not confer ampicillin resistance. Eukaryotic cDNA libraries cloned into pCAST produced tens of thousands of ampicillin-resistant clones, 80% of which contained cDNA fragments encoding secreted and membrane spanning proteins. We identified 2,708 unique sequences from cDNA libraries made from surgical breast cancer specimens. We analyzed the expression of 1,287 of the 2,708 genes and found that 166 were overexpressed in breast cancers relative to normal breast tissues. Eighty-five percent of these genes had not been previously identified as markers of breast cancer. Twenty-three of the 166 genes (14%) were relatively tissue restricted, suggesting use as cancer-specific targets. We also identified several new markers of ovarian cancer. Our results indicate that CAST is a robust, rapid, and low cost method to identify cell surface and secreted proteins and is applicable to a variety of relevant biological questions.

Ampicillin Resistance↗
PubMed1987

Autonomic nervous control of fundic secretion of somatostatin and antral secretion of gastrin and somatostatin in pigs.

By selective catheterization of gastric veins, we studied the secretion of gastrin and somatostatin from the antrum and of somatostatin from the gastric fundus-corpus region in anaesthetized pigs with or without acute adrenalectomy. The secretion was studied during electrical stimulation of the vagus nerves and the splanchnic nerves and simultaneous irrigation of gastric lumen with fluids of high, low, and neutral pH. The corpus-fundus somatostatin response to vagal stimulation was biphasic with a short-lasting initial increase followed by a lasting inhibition, which was little influenced by intraluminal pH or adrenalectomy. In pigs with intact adrenals, antral somatostatin secretion was increased by vagal stimulation, whereas in adrenalectomized pigs, the effect was inhibitory. The vagally induced inhibition was abolished when the intragastric pH was kept at pH 2. The antral gastrin secretion was strongly stimulated by vagal stimulation. The magnitude of the secretory response was inversely related to the pre-stimulatory somatostatin levels, but not to the nerve stimulation responses. Splanchnic stimulation increased arterial blood pressure and gastric blood flow, but had inconsistent effects on somatostatin and gastrin secretion.

Adrenalectomy↗
PubMed1983

Adrenocorticotropin secretion by mouse pituitary tumor cells in culture: the role of Ca+2 in stimulated and somatostatin-inhibited secretion.

SRIF inhibits ACTH secretion by AtT20/D16v (D16) mouse pituitary cells stimulated by high (50 mM) extracellular concentrations of K+ or by divalent cation ionophores. Although stimulation of ACTH secretion by K+ requires extracellular Ca+2, the response is invariant over medium Ca+2 concentrations of 0.003-1 mM; with Ca+2 concentrations from 1-5 mM there is a dramatic amplification of the secretory response. SRIF at concentrations of 10(-8) M completely inhibits the secretory response to K+ at Ca+2 concentrations between 0.2 and 1 mM; with increasing medium Ca+2 above 1 mM there is a progressive attenuation of SRIF-inhibition. At concentrations of 5 mM, Ca+2 alone can serve as an ACTH secretagogue. The ionophore ionomycin stimulates ACTH secretion in a Ca+2-dependent manner with a half-maximal effect at 5 X 10(-6) M ionomycin. The secretory response to ionomycin and to X537A is inhibited by at least 50% by SRIF. The secretory response to K+ is accompanied by a rapid and sustained increase in 45Ca+2 uptake, whereas the ionophores ionomycin, X537A, and A23187 increase Ca+2 efflux. SRIF does not affect Ca+2 movement across D16 cell membranes in response to either K+ or ionophores. These results show that an increase in intracellular Ca+2 is an effective stimulus to ACTH secretion by D16 cells and inhibition of ACTH secretion by SRIF is not effected by interference with the stimulus-elicited increase in intracellular Ca+2.

Adrenocorticotropic Hormone↗
PubMed1987

Antiestrogen stimulation of the production of a 37,000 molecular weight secreted protein and estrogen stimulation of the production of a 32,000 molecular weight secreted protein in MCF-7 human breast cancer cells.

Antiestrogens (AE), such as tamoxifen, selectively increase the production of a secreted protein of 37,000 mol wt (Mr) in estrogen receptor-containing human breast cancer cells (MCF-7, but not in estrogen receptor-negative MDA-MB-231 cells), and the production of this protein by AE is inhibited by concomitant estradiol (E) treatment. Likewise, E increases the production of a 32,000 Mr secreted protein whose synthesis is inhibited by AE. Proteins were detected by [35S]methionine and [35S]cysteine labeling of cells and analysis of proteins by sodium dodecyl sulfate-polyacrylamide gels and fluorography. Enhanced production of the 37,000 Mr protein is observed within 6 h of AE treatment, with maximal synthesis seen at 1-2 days when this protein represents about 6% of the total radiolabeled secreted proteins. This protein is stimulated maximally (approximately 4-fold) by 10(-8) M trans-hydroxytamoxifen or LY117018 or 10(-6) M tamoxifen, and its AE specificity is seen by the fact that trans-tamoxifen increases this protein, whereas cis-tamoxifen, an estrogen, does not. In addition to stimulating the synthesis of previously identified 160,000 and 52,000 Mr secreted proteins, E increases the production of a 32,000 Mr secreted protein. When cells are grown in estrogen-free conditions, i.e. in charcoal-dextran-treated serum in medium lacking the estrogen phenol red, the basal level of the 32,000 Mr protein is extremely low, and E stimulation results in a 10-fold increase in the production of this protein, with increases observable by 6 h and maximal stimulation at 2 days. Interestingly, the basal level of synthesis of the 37,000 Mr protein is high in the absence of E and is then stimulated only minimally by the addition of AE, suggesting that this protein is clearly produced as an estrogen-antagonistic protein. Amino acid incorporation conducted in the presence of tunicamycin and endoglycosidase H indicates that both of these proteins are glycoproteins. These proteins should serve as useful markers for AE and E action and may be involved in AE and E modulation of cell proliferation and/or cell function.

Amino Acids↗
PubMed1989

Regulation of prolactin secretion in the human B-lymphoblastoid cell line IM-9-P3 by dexamethasone but not other regulators of pituitary prolactin secretion.

We examined whether the ectopic production of human(h) PRL by the human B-lymphoblastoid cell line IM-9-P3 is under hormonal control. We demonstrate that PRL secretion in this cell line is regulated by dexamethasone but not by other hormones known to modulate PRL secretion in the pituitary or decidua. Dexamethasone caused a reduction of secretion rates to 30% of control values after 3 day paralleled by a decrease in hPRL mRNA levels, without affecting cell viability. Half-life determinations of hPRL mRNA in control and dexamethasone-treated cells revealed a reduction of t1/2 from 16 to 4 h. PRL secreted by IM-9-P3 cells did not control its own secretion in an autocrine loop, nor did it serve as an autocrine growth factor.

Antibodies, Monoclonal↗
PubMed1997

Neuroendocrine control of follicle-stimulating hormone (FSH) secretion. I. Direct evidence for separate episodic and basal components of FSH secretion.

Continuous sampling of hypophyseal portal blood from unrestrained sheep is providing an unprecedented means for measuring and defining the characteristics of the secretory profile of GnRH. With this method, GnRH has been shown to be released in discrete pulses lasting 5-8 min, with the amplitude of some pulses exceeding 50-fold. Although the relationship between these pulses and the accompanying pulses of LH measured in the jugular vein are unambiguous, the relationship of GnRH pulses to the release of FSH has not been well defined due to the longer clearance of FSH. In previous studies we have shown that hypophyseal portal blood, in addition to serving as a source material for hypothalamic secretions, provides a means to define secretory patterns of pituitary hormones. Because of this we hypothesized that the GnRH-FSH secretory relationship would be easier to define in hypophyseal portal than in jugular vein blood before the secretory products are subjected to dispersion and clearance in circulation. To test this possibility, we monitored hormonal patterns in blood collected at 5-min intervals for 6-12 h from the peripheral and hypophyseal portal circulation of six ovariectomized ewes from a previous study. In contrast to the nonpulsatile pattern of FSH in the peripheral blood, 93% of the GnRH pulses were associated with essentially coincident, discrete pulses of FSH in the portal plasma. Of potentially even greater interest, additional episodes of FSH release were clearly discernible between the GnRH-associated pulses of FSH. As concentrations of peripheral plasma FSH did not reach those in hypophyseal portal plasma, the inter-GnRH episodes of FSH secretion could not result from contaminating peripheral blood. In addition to the episodic mode of secretion, substantial amounts of FSH were found between FSH pulses. This basal component of FSH appeared to be the dominant mode of secretion rather than pulses. The results of this study not only confirm that GnRH pulses lead to pulsatile release of FSH, they also suggest that some other mechanism or factor may be controlling the non-GnRH-associated episodes as well as the basal components of FSH secretion.

Animals↗
PubMed1984

The role of endogenous opiates in the mechanism of inhibited luteinizing hormone (LH) secretion in women with anorexia nervosa: the effect of naloxone on LH, follicle-stimulating hormone, prolactin, and beta-endorphin secretion.

The aim of this study was to evaluate the role of endogenous opiates in the mechanism of decreased LH secretion in women with anorexia nervosa. For this purpose the effect of opiate receptor blockade with naloxone on LH, FSH, PRL, and beta-endorphins secretion was studied in 24 women with anorexia nervosa and 7 normal women. Serum LH, FSH, PRL, beta-endorphin-like substance, ACTH, and cortisol concentrations were measured before and after opiate receptor blockade after a single iv dose of 0.2 mg/kg naloxone or saline. Mean serum LH and FSH concentrations increased significantly after naloxone in the normal women. Eleven patients had a significant increase in serum LH concentrations in response to naloxone and 13 did not respond to naloxone with an increase in LH concentration. In the first group the basal LH values were higher than those in the second group. In the majority of patients in the first group amenorrhea preceded the wt loss, whereas in most patients in the second group amenorrhea appeared during the phase of wt loss. Naloxone did not alter pulsatile LH secretion in 6 women. No effect of naloxone on serum FSH and PRL concentrations was found. A significant increase in beta-endorphin-like substance levels after naloxone administration occurred in patients with anorexia nervosa. However, serum ACTH and cortisol concentrations were not altered in response to naloxone. In conclusion, the increase in LH release after opiate receptor blockade by naloxone suggests that endogenous opiates may play a role in the mechanism of inhibited LH secretion at least, in the majority of those women with anorexia nervosa in whom amenorrhea preceded wt loss. The results also point to a different mechanism of ACTH and beta-endorphin secretion in patients with anorexia nervosa.

Adolescent↗
PubMed1985

Parathyroid hormone secretion from dispersed human hyperparathyroid cells: increased secretion in cells from hyperplastic glands versus adenomas.

The in vitro secretion of PTH by dispersed human parathyroid cells was examined under conditions of low and high extracellular Ca+2 using tissue from patients with primary hyperparathyroidism and hyperparathyroidism resulting from chronic renal failure (CRF). The PTH secretion rate (nanograms of PTH per 10(5) cells/h) was lower in adenomatous tissues than in either primary hyperplastic cells or CRF cells under conditions of low (0.5 mM) or high (2.0-3.0 mM) extracellular Ca+2. Among the adenomas, a wide spectrum of degree of suppressibility of PTH secretion by high Ca+2 was found, ranging from 0% (completely nonsuppressible) to 98%. Suppression of the hyperplastic tissues in general was similar. The most suppressible adenomas demonstrated 2-fold greater PTH secretion rates in low Ca+2 conditions than the least suppressible adenomas, but in high Ca+2 conditions, the two groups had similar secretory rates. We conclude that the rate of PTH secretion by cells from adenomas was substantially lower than that of cells from tissues exhibiting either primary hyperplasia or hyperplasia resulting from CRF under these in vitro conditions. Thus, in adenomas, an increase in absolute cell number as well as alterations in the degree of calcium responsiveness may prove to be important etiological factors in the expression of hyperparathyroidism.

Adenoma↗
PubMed1987

The effects of bromocriptine, thyrotropin-releasing hormone, and gonadotropin-releasing hormone on hormone secretion by gonadotropin-secreting pituitary adenomas in vivo and in vitro.

The characteristics and dynamics of hormone secretion in vivo and in vitro were investigated in six patients with gonadotropin-secreting pituitary adenomas. All six tumors secreted and contained FSH and different combinations of LH, beta-LH, and alpha-subunit. In addition, immunohistochemical examination of the pituitary tumor tissue showed staining with both LH and FSH in three and either LH or FSH in the other three tumors. TRH and GnRH stimulated hormone secretion in vivo and in vitro, and they also increased the hormone content of the cultured tumor cells. Bromocriptine significantly inhibited hormone release and reduced the hormone content of the tumor cells. In vivo, 2.5 mg bromocriptine significantly suppressed plasma hormone levels; the inhibiting effect on alpha-subunit concentrations was in general more marked than that on LH and FSH. We conclude that hormone release by gonadotropin-secreting pituitary adenomas can be stimulated by TRH and GnRH and inhibited by bromocriptine. Most of these tumors synthesize FSH, but there is a wide variation in the production of LH, beta-LH, and alpha-subunits. The sensitivity of hormone release to bromocriptine suggests that chronic therapy with this drug might have a beneficial effect on pituitary tumor size.

Adenoma↗
PubMed1994

Hypothalamic-pituitary-adrenal axis activation and stimulation of systemic vasopressin secretion by recombinant interleukin-6 in humans: potential implications for the syndrome of inappropriate vasopressin secretion.

We recently demonstrated that sc administered interleukin-6 (IL-6) strongly stimulates the human hypothalamic-pituitary-adrenal (HPA) axis, with mild toxicity and no hypotensive effects. In this study, we evaluated the response of the human HPA axis to escalating iv doses of recombinant IL-6 in six patients with cancer and good performance status who received daily, every 8 h, three equal doses of 0.3-30 micrograms/kg IL-6. The plasma levels of IL-6 assayed by a specific enzyme-linked immunosorbent assay during the 4 h following the first IL-6 injection were elevated for 2-4 h, proportionally to the amount of injected IL-6. Administration of the cytokine was followed by marked elevations of plasma ACTH (53.0-98.6 pmol/L) and cortisol (824.9-1729.9 nmol/L) independently of the IL-6 dose administered, suggesting that the doses employed were at the top of the dose-response curve for these hormones. Interestingly, plasma arginine vasopressin (AVP) levels were also elevated during the 2 h after IL-6 injection in all patients who received a dose of 3 micrograms/kg or more, suggesting that IL-6 activated the magnocellular AVP-secreting neurons and that it might be involved in the syndrome of inappropriate AVP secretion. Cortisol elevations with peaks similar to those observed after the first injection of IL-6 were also detected in plasma sampled every 2 h after the second and third injections, suggesting that there was no rapid tachyphylaxis in response to IL-6 administration. Plasma IL-1 beta and tumor necrosis factor-alpha concentrations, assayed by specific enzyme-linked immunosorbent assays during the 4 h after the first IL-6 injection, were either within the normal range or undetectable, confirming in vitro observations that IL-6 does not stimulate IL-1 beta or tumor necrosis factor-alpha secretion and suggesting that it exerts its effect on the HPA axis and AVP secretion independently of them. We conclude that IL-6 is a potent stimulator of the human HPA axis and a secretagogue of magnocellular AVP secretion, which might be employed as a challenge test of the axis and the magnocellular AVP neuron.

Adrenocorticotropic Hormone↗
PubMed2001

Differential regulation of gonadotropin secretion by testosterone in the human male: absence of a negative feedback effect of testosterone on follicle-stimulating hormone secretion.

Studies of sex steroid regulation of gonadotropin secretion in the human male have focused primarily on the respective site(s) of negative feedback of testosterone (T) and estradiol (E(2)). The use of pharmacological doses of sex steroids in these studies has precluded conclusions about the relative roles of T and E(2) in gonadotropin feedback. Thus, the aims of the present study were to 1) determine the relative contributions of T vs. E(2) to the sex steroid component of gonadotropin regulation, and 2) distinguish the feedback effects of T that that are direct (i.e. mediated by the androgen receptor) vs. indirect (mediated by aromatization to E(2)). Two experimental interventions were used: 1) inhibition of aromatization by a selective aromatase inhibitor to examine the impact of selective E(2) withdrawal; and 2) acute medical castration to examine the effect of ablating both T and E(2). Sixteen normal (NL) men (mean age, 30.5 +/- 2.2 yr) were studied. Nine NL subjects were treated with the aromatase inhibitor, anastrozole (10 mg, orally, daily, for 5 days). Twelve NL men underwent medical castration with ketoconazole (1-g loading dose followed by 400 mg, orally, four times a day for 5 days). Ketoconazole-treated subjects received concomitant treatment with dexamethasone (0.5 mg twice daily) to prevent the development of adrenal insufficiency. Single blood samples were drawn daily between 0800-1000 h. To ensure that dexamethasone was not altering the gonadotropin response to sex steroid ablation by a direct pituitary effect, five GnRH-deficient men (mean age, 37.6 +/- 3.9 yr) underwent GnRH dose-response studies at baseline and after treatment with dexamethasone (0.5 mg twice daily). Aromatase blockade caused significant lowering of E(2) (33 +/- 3 to 14 +/- 1 pg/mL; P: < 0.0005) with a corresponding increase in T levels (563 +/- 42 to 817 +/- 81 ng/dL; P: < 0.05). Treatment with ketoconazole resulted in equivalent suppression of E(2) (41 +/- 4 to 14 +/- 1 pg/mL; P: < 0.0005), but also induced castrate levels of T (491 +/- 28 to 40 +/- 3 ng/dL; P: < 0.0005). Both treatment regimens were associated with a significant increase in gonadotropin levels. For LH, the percent increase in serum levels after castration was almost 3-fold greater than that seen after selective E(2) withdrawal (275 +/- 23% with ketoconazole vs. 95.6 +/- 21% with anastrozole; P: < 0.005). Despite the divergent changes in T levels with these two maneuvers (a marked decrease after ketoconazole and a significant increase with anastrozole), the percent rise in FSH levels was similar in the two protocols (91 +/- 6% vs. 71 +/- 7%, respectively; P: = NS). Inhibin B levels were unchanged after selective E(2) withdrawal (156 +/- 23 vs. 176 +/- 19 pg/mL), but decreased slightly with ketoconazole (156 +/- 15 to 131 +/- 11 pg/mL; P: < 0.05). In contrast to the effects of glucocorticoid administration on gonadotropin secretion in women, no significant changes were observed in the GnRH-deficient men treated with dexamethasone in terms of mean LH levels (19.8 +/- 3.2 vs. 23.3 +/- 5.4 IU/L), mean LH pulse amplitude after GnRH (16.0 +/- 2.5 vs. 19.0 +/- 5.1 IU/L), or mean FSH levels (8.0 +/- 1.9 vs. 9.2 +/- 2.4 IU/L, pre vs. post). These studies provide evidence of differential regulation of gonadotropin secretion by T in the human male. T exerts both direct and indirect feedback on LH secretion, whereas its effects on FSH appear to be mediated largely by aromatization to E(2). From these data we conclude that in terms of sex steroid feedback, E(2) is the predominant regulator of FSH secretion in the human male.

Adult↗
PubMed1991

Growth hormone secretion patterns in relation to LH and estradiol secretion throughout normal female puberty.

Pulsatile growth hormone secretion patterns were studied in relation to luteinizing hormone and estradiol release in 33 healthy (pre)pubertal girls. Plasma GH was determined every 10 min, plasma LH and E2 every hour. Night-time GH release was always higher than daytime GH release. During daytime, all GH secretion parameters, except for the basal GH level, increased significantly from the prepubertal stage to stage B4 before (m-) the menarche (p = 0.05) and decreased thereafter (p = 0.05). During night-time, mean GH level and the fraction of GH in pulses also tended to increase from stage B1 to stage B4m-. The number of high pulses (greater than 8 micrograms/l) during day and night together tended to increase until stage B4m- and decreased after the menarche (p = 0.05). Height velocity did not correlate with the number of high pulses (Kendall tau = 0.14, p = 0.14). From stage B1 to B4m- high correlations were observed between E2 levels and GH secretion parameters, particularly during the day (tau = 0.59-0.71, p less than or equal to 0.01). The correlations between LH levels and GH secretion were high as well (tau = 0.50-0.81, p less than or equal to 0.01), but equal during day and night. It is concluded that during puberty 1. spontaneous GH release in girls increases 2-3 fold until the menarche and decreases thereafter, primarily as the result of an increasing and decreasing GH pulse amplitude; 2. diurnally increasing estradiol levels correlated with increasing GH secretion.

Adolescent↗
PubMed1987

Opiate suppression of LH secretion involves central receptors different from those mediating opiate effects on prolactin secretion.

The involvement of mu- and kappa-opiate receptors in the regulation of LH and prolactin secretion was investigated in long-term ovariectomized rats using selective opiate receptor agonists and antagonists. The mu-agonists morphine and [D-Ala2,MePhe4,Gly5-ol]-enkephalin (DAGO) suppressed LH levels in a dose-related manner. The benzomorphane (-)-5,9-dimethyl-2'-hydroxy-2-(tetrahydrofurfuryl)-6,7-benzomorphan tartrate (MR 2034; a designated kappa-agonist) also suppressed LH levels, whereas another benzomorphane kappa-agonist (-)-5,9-dimethyl-2'-hydroxy-2-(2-methoxy-propyl)-6,7-benzomorphan hydrobromide (MRZ 2549) had no effect on the levels of this hormone. Pretreatment with the highly selective mu-antagonist beta-funaltrexamine (beta-FNA), the fumarate methyl ester derivative of naltrexone, blocked the actions of both mu-agonists and MR 2034, indicating that opiate suppression of LH secretion is mediated by mu-receptors. This was further confirmed by in-vitro studies: the KCl-induced release of LHRH from perifused hypothalami obtained from ovariectomized rats was significantly reduced by DAGO but not by MRZ 2549. Prolactin secretion was stimulated in a dose-dependent manner by both mu- and kappa-agonists. The stimulation caused by morphine and DAGO was antagonized by beta-FNA, whereas that caused by the kappa-agonists MR 2034 and MZR 2549 was resistant to blockade by beta-FNA but not by naloxone (an antagonist which blocks all classes of opiate receptors when given in high doses). Thus prolactin secretion seems to be regulated by both mu- and kappa-opiate receptors, whereas the effects on LH secretion seem to involve mu-receptors only.

Animals↗
PubMed1990

Involvement of the adrenal gland in the suckling-induced decrease in LH and FSH secretion and the concomitant increase in prolactin secretion in the rat.

The role of the adrenal gland in the regulation of gonadotrophin and prolactin secretion in the lactating rat was investigated. Changes in secretion of LH, FSH, prolactin, ACTH, beta-lipotrophin (beta-LPH), inhibin, corticosterone and progesterone after adrenalectomy were examined during the second half of lactation. Follicular maturation was determined by the ability of the follicles to ovulate in response to 10IU human chorionic gonadotrophin (hCG). Adrenalectomy on day 10 of lactation prevented an increase in plasma concentrations of LH and FSH in response to ovariectomy performed at the same time as adrenalectomy, and markedly stimulated secretion of ACTH, beta-LPH and prolactin. Adrenalectomy reduced the number of follicles capable of ovulating in response to hCG. Concentrations of inhibin and progesterone in the plasma significantly decreased after adrenalectomy, indicating that development of ovulatory follicles and luteal function had been suppressed. Abolishing the increase in plasma concentrations of LH and inducing a decrease in FSH in the plasma by adrenalectomy therefore prevented maturation of a new set of follicles usually seen during the second half of lactation in rats. The decrease in plasma concentrations of LH also inhibited the ability of the corpus luteum to secrete progesterone, although high concentrations of plasma prolactin were maintained in adrenalectomized lactating rats. These results indicate that the pituitary-adrenal system is capable of influencing the maintenance of a normal secretion of gonadotrophin and prolactin as well as the maintenance of ovarian function during lactation in the rat.

Adrenal Glands↗
PubMed1979

The hepatic secretion of lecithin: cholesterol acyltransferase in rats with increased secretion of triglycerides due to ventromedial hypothalamic lesions.

Lecithin:cholesterol acyltransferase (LCAT) is postulated to take care of excess cholesterol formed during metabolism of triglyceride (TG)-rich lipoproteins. To test this hypothesis the relationship between secretion of LCAT and TG have been investigated in rats with ventromedial hypothalamic lesions which lead to increased hepatic secretion of TG. 1. The increased plasma concentration of TG in rats with ventromedial hypothalamic lesions was positively correlated to the activity of LCAT in plasma. 2. Incubation of hepatocytes isolated from such rats revealed a positive linear correlation between secretion of TG and of LCAT. 3. The secretion of unesterified cholesterol was neither correlated to the secretion of the acyltransferase nor to the TG.

Animals↗
PubMed1993

Motility-related cyclic fluctuations of interdigestive gastric acid and bicarbonate secretion in man. A source of substantial variability in gastric secretion studies.

The relationship between interdigestive gastric motility and secretion was studied in eight healthy volunteers. Acid and bicarbonate output rates were measured with a high time resolution, using a perfusion system based on continuous registration of pH and PCO2 of gastric effluent. Antral pressure was measured by manometry. The total duration of the interdigestive motility cycle (time between two phase-III complexes) was 96 +/- 12 min (mean +/- SE). In late migrating motor complex phase II, acid output, bicarbonate output, and bile reflux increased significantly. Acid secretion reached a peak in association with motor phase III. The gastric lumen was then rapidly alkalinized; this phenomenon was due to a simultaneous decrease in acid secretion and a short-lasting (15 +/- 2 min, mean +/- SE) phasic increase in bicarbonate output, which was not associated with bile reflux (bilirubin). After these phase-III-related events both acid and bicarbonate output rates reached a relatively stable level during phase I and early phase II. This period of stability constituted 47 +/- 3% (acid) and 41 +/- 6% (bicarbonate, means +/- SE), respectively, of the cycle. The peak to base line output ratio was 6.6 +/- 1.2 (p < 0.001) for acid and 2.8 +/- 0.3 (p < 0.001) for bicarbonate (means +/- SE). The results show a marked variability in acid and bicarbonate output rates during the interdigestive motility cycle. The magnitude of this variability has previously been underestimated owing to poor time resolution of the secretion measurements. If not taken into account, these 'spontaneous' secretory variations may constitute a considerable source of error in gastric secretion studies.

Adult↗