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At least 541 records · Page 30Linked to original sources
PubMed2003

Neuroendocrine control of follicle-stimulating hormone (FSH) secretion: III. Is there a gonadotropin-releasing hormone-independent component of episodic FSH secretion in ovariectomized and luteal phase ewes?

Our previous studies in ovariectomized ewes have provided direct evidence that FSH secretion is comprised of basal and episodic modes. In those studies, each GnRH pulse coincided with an FSH pulse, but additional FSH pulses were noted. To determine whether non-GnRH-associated pulses of FSH represent a GnRH-independent component of FSH secretion, we determined whether episodic FSH secretion persists after blockade of GnRH action with a GnRH antagonist. Hypophyseal portal and jugular blood was collected from five ovariectomized and six luteal phase ewes at 5-min intervals for 6 h before and 6 h after a single iv injection of Nal-Glu (10 micro g/kg body weight). Hypophyseal portal LH and FSH and jugular patterns of FSH were compared with patterns of GnRH. Before Nal-Glu, in both models, there was a one-to-one concordance between GnRH and portal LH pulses, and each GnRH pulse was associated with a FSH pulse. However, additional non-GnRH-associated pulses of FSH were present. Nal-Glu administration eliminated LH but not FSH pulsatility. Nal-Glu inhibited interaction of GnRH I with GnRH type I receptor but not interaction of GnRH II with type II receptor. These studies provide the first direct evidence of the existence of an acute GnRH I-independent component of episodic FSH secretion.

Animals↗
PubMed2005

Functional expression of beta-chemokine receptors in osteoblasts: role of regulated upon activation, normal T cell expressed and secreted (RANTES) in osteoblasts and regulation of its secretion by osteoblasts and osteoclasts.

The expression and functions of receptors for the beta-chemokine, regulated upon activation, normal T cell expressed, and secreted (RANTES)/CCL5, were investigated in osteoblasts. Both primary osteoblasts and the MC3T3-E1 osteoblast cell line express the RANTES receptors, CCR1, 3, 4, and 5 (by RT-PCR), which encode functional receptors in osteoblasts as shown by [125I]-RANTES binding followed by Scatchard analysis. Expression of all four RANTES receptor mRNAs in osteoblast is in contrast to the reports of expression of CCR1 being the only RANTES receptor expressed by osteoclasts. Exogenous RANTES elicits chemotaxis of osteoblasts and promotes cell survival via phosphatidylinositol 3-kinase with attendant phosphorylation of Akt. Osteoclastic RANTES, obtained from the conditioned medium of receptor activator of nuclear factor-kappa B ligand-differentiated RAW264.7 cells also induces chemotaxis of MC3T3-E1 cells. Incubating the conditioned medium with an anti-RANTES neutralizing antibody attenuated this effect. RANTES secretion from osteoblast is inhibited by differentiation promoting hormones, e.g. 1,25 (OH)2D3 and dexamethasone, whereas macrophage inflammatory protein-1 alpha (but not macrophage inflammatory protein-1 beta) and elevated calcium induce it. Elevated calcium also stimulated RANTES secretion by osteoclasts. Therefore, RANTES is an osteoblast chemoattractant and a survival-promoting molecule whose regulation in osteoblast is varied. Furthermore, RANTES secreted from osteoclasts induces osteoblast chemotaxis. Therefore, expression of RANTES and its receptors in both osteoblasts and osteoclasts could enable this chemokine to act in autocrine/paracrine modes.

Animals↗
PubMed1989

Time course of hepatic 3-hydroxy-3-methylglutaryl coenzyme A reductase activity and messenger ribonucleic acid, biliary lipid secretion, and hepatic cholesterol content in methimazole-treated hypothyroid and hypophysectomized rats after triiodothyronine administration: possible linkage of cholesterol synthesis to biliary secretion.

In an effort to define the mechanism by which thyroid hormone increases the synthesis of hepatic cholesterol, we have investigated both in hypophysectomized and methimazole-treated hypothyroid rats the time course of T3 effects on plasma cholesterol concentration, total hepatic cholesterol, the rate of biliary secretion of cholesterol, bile acids, and phospholipids, and the activity and mRNA levels of 3-hydroxy-3-methylglutaryl coenzyme-A (HMG-CoA) reductase, the rate-limiting enzyme in the hepatic synthesis of cholesterol. A single dose of 200 micrograms T3 was estimated to maintain at least 90% nuclear occupancy for the ensuing 54 h of the experiment. In both preparations the relative rise in biliary secretion of cholesterol exceeded that of other biliary constituents and preceded by 12 h an increase in HMG-CoA reductase enzyme activity and its mRNA. The level of total hepatic cholesterol remained constant throughout the experiment. We interpret these findings to suggest that T3-stimulated cholesterol synthesis is mediated by an antecedent T3-induced rise in biliary cholesterol secretion. We postulate that biliary cholesterol secretion is augmented by an intrahepatic shift of cholesterol and depletion of the hepatic sampling center responsible for the feedback regulation of cholesterol synthesis. The level of HMG CoA reductase mRNA appeared to govern enzyme activity in both preparations, but the ratio of mRNA to hepatic enzyme activity was substantially greater in the methimazole-treated compared with the hyphophysectomized animals.

Animals↗
PubMed2004

Augmentation of growth hormone secretion after testosterone treatment in boys with constitutional delay of growth and adolescence: evidence against an increase in hypothalamic secretion of growth hormone-releasing hormone.

The increase in pituitary GH secretion that occurs during mid-late puberty in boys follows an increase in circulating testosterone (T) concentration; the direct mechanism by which this occurs is unknown. We hypothesized that T increases GH secretion during puberty by augmenting hypothalamic output of GHRH. Using constant infusions of a GHRH antagonist, we tested this hypothesis in six early pubertal boys with constitutional delay of growth and adolescence who had a mean chronological age of 14.0 +/- 0.3 yr and mean bone age of 11.4 +/- 0.2 yr. Blood samples were obtained from subjects every 15 min for 24 h during the overnight infusion of normal saline (2000-0600 h) and again during the overnight infusion of GHRH antagonist (0.33 microg/kg/h) the following night. Subjects then received transdermal T (5-mg patch) for 12 h nightly and were studied again after 4 wk of treatment. Serum samples were assayed for GH and total ghrelin; the percent suppression of GH during GHRH antagonist infusion was calculated. Morning serum T rose from 0.44 +/- 0.09 to 4.43 +/- 0.74 microg/liter (P = 0.005). T treatment was associated with a 92.6% increase in mean nocturnal GH secretion area under the curve (830 +/- 177 to 1599 +/- 340 microg/24 h.liter). Infusion of GHRH-antagonist suppressed mean nocturnal GH area under the curve by 29.1% before T treatment (830 +/- 177 to 621 +/- 168 microg/24 h.liter), and by 29.4% after T treatment (1599 +/- 340 to 1182 +/- 249 microg/24 h.liter; P = 0.99). Somatotroph sensitivity to GHRH was tested with 0.1- and 1.0-microg/kg doses of GHRH-44 iv; GH response did not change with regard to T treatment. The mean 24-h concentration of total ghrelin was unchanged with regard to T treatment. In summary, nightly transdermal T administration in six boys with constitutional delay of growth and adolescence increased GH output almost 2-fold, whereas the degree of GH suppressibility by GHRH antagonist remained unchanged. We conclude that the T-associated augmentation of GH secretion during early puberty in boys is unlikely to involve an absolute increase in hypothalamic GHRH output.

Adolescent↗
PubMed2005

Preproorexin and orexin receptors are expressed in cortisol-secreting adrenocortical adenomas, and orexins stimulate in vitro cortisol secretion and growth of tumor cells.

Orexins A and B are hypothalamic peptides that originate from the proteolytic cleavage of preproorexin and act through two subtypes of receptors, named OX1-R and OX2-R. OX1-R almost exclusively binds orexin-A, whereas OX2-R is nonselective for both orexins. We previously found that orexin-A, via the OX1-R, stimulates cortisol secretion from dispersed human adrenocortical cells. In this study, we demonstrate that six of eight cortisol-secreting adenomas expressed preproorexin mRNA, and seven of 10 adenomas contained measurable amounts of orexin-A but not orexin-B. Normal adrenal cortexes neither expressed preproorexin nor contained orexins. All adenomas expressed OX1-R and OX2-R mRNAs, and real-time PCR showed that the expression of both receptors was up-regulated in adenomas, compared with normal adrenal cortex. Orexin-A concentration-dependently raised basal cortisol secretion from freshly dispersed normal and adenomatous cells, minimal and maximal effective concentrations being 10(-10) and 10(-8) m, and the peptide efficacy (percent increase elicited by 10(-8) m orexin-A) was significantly higher in adenomas than in the normal adrenal cortex. Orexin-B was ineffective, thereby indicating that orexin secretagogue action is mediated by the OX1-R. In contrast, both orexins (10(-8) m) raised the proliferative activity of cultured normal and adenomatous cells, suggesting that this effect is mediated by OX2-R or both receptor subtypes. Collectively, our findings allow us to conclude that the orexin system is overexpressed in cortisol-secreting adenomas and suggest that orexin-A may act as an autocrine-paracrine regulator of the secretory activity and growth of some of these adrenal tumors.

Adrenal Cortex Neoplasms↗
PubMed1984

Pulsatile gonadotropin secretion during the human menstrual cycle: evidence for altered frequency of gonadotropin-releasing hormone secretion.

Pulsatile secretion of LH and FSH was examined to determine if the frequency of LH pulses, and by inference pulsatile GnRH secretion, varied during the human menstrual cycle. Blood samples were obtained at 10- or 20-min intervals for 12 or 24 h at 7-day intervals during the same ovulatory cycle in eight normal women. Ovarian steroids showed the expected cyclical changes and mean plasma FSH concentrations showed an inverse relationship to estradiol, being low when estradiol was greater than 150 pg/ml. Sampling every 10 min revealed a constant LH pulse amplitude but LH pulse frequency increased (from 11.8 to 14.3 pulses/12 h) during the follicular phase. LH pulse frequency was not further increased in two women sampled during the LH surge, but pulse amplitude was markedly higher. During the luteal phase LH pulse frequency was reduced to eight pulses/12 h but frequency was more variable between subjects than in the follicular phase. LH pulse amplitude showed striking variation (0.8-29.4 mIU/ml) during the luteal phase of the cycle and large LH secretory episodes which lasted 1-3 h were irregularly interspersed among periods of low amplitude LH secretion. These data show that the frequency of LH pulses, and by inference GnRH secretion, varies during the menstrual cycle but the degree of change is less than reported in previous studies. This observation may explain the reported efficacy of fixed frequency GnRH regimes in inducing ovulation and cyclical ovarian function.

Adult↗
PubMed1988

Gonadotropin-releasing hormone agonists are unsuccessful in reducing tumoral gonadotropin secretion in two patients with gonadotropin-secreting pituitary adenomas.

Whether GnRH agonist treatment leads to reduced gonadotropin secretion and tumor volume in patients with gonadotropin-secreting pituitary adenomas is controversial. We studied the effect of GnRH analog treatment in two such patients, one with a recurrent FSH- and LH-secreting pituitary adenoma (patient 1) and one with a recurrent FSH- and alpha-subunit-secreting pituitary adenoma (patient 2). Patient 1 was treated with 200 micrograms Buserelin daily for 65 days, and patient 2 received three injections of 3 mg [D-Trp6]-LHRH formulated in microcapsules at 21-day intervals. In both patients, plasma FSH, LH (RIA), and alpha-subunit concentrations increased initially and remained above the pretreatment values throughout the treatment period. Plasma LH, measured by immunoradiometric assay, remained well above the detection limit. Plasma bioactive LH and testosterone became undetectable in patient 2, but did not change in patient 1. In neither patient did pituitary tumor size (determined by computed tomographic scan) change during treatment. We conclude that 1) the overall effect of GnRH analogs in patients with gonadotroph cell adenomas is stimulation of gonadotropin release by the tumor, although LH release varies according to how plasma LH is measured, possibly related to the origin of the hormone (normal or tumor gonadotroph cells), and 2) GnRH analog treatment does not reduce tumor size.

Adenoma↗
PubMed1981

The secretion of the eggshell of Schistocerca gregaria, analysis of the kinetics of secretion in vitro by light and electron microscope autoradiography.

The secretion of the 2 main layers (endochorion and exochorion) of the eggshell of the desert locust Schistocerca gregaria was investigated using light and electron microscope autoradiography. Follicles undergoing endochorion secretion were labelled using a 3 min 'pulse' of [3H]leucine in vitro followed by a 0-115 min non-radioactive 'chase'. Immediately after the pulse the silver grains were distributed over the cytoplasm and organelles including rough endoplasmic reticulum, while by 2 and 5 min Golgi bodies contained radioactivity. By 12 min from the beginning of the chase the cell apex containing small secretory vesicles was labelled. By 20 min most of the silver grains were over the endochorion. The half-transport time (t50) was 14--15 min (from mid pulse), the lag time was 9--10 min and the percentage transport rate was 14--15% per min. When a 3 min pulse of [3H]galactose was used to label exochorion precursors, the shorter t50 (11 min) and the clumped grain distribution in light microscope autoradiographs after 0-min chase suggested that galactose was incorporated in Golgi bodies. The secretion of exochorion precursors appears to occur at a similar rate to that of endochorion precursors (approximately 15% per min). The results indicate that the follicle cells are among the fastest secreting cells.

Animals↗
PubMed1992

[Effects of ambroxol HCl on the guinea pig tracheal mucous secretion and the rat pulmonary surfactant secretion].

The effects of orally administered ambroxol HCl (ambroxol) on guinea pig tracheal mucous secretion and rat pulmonary surfactant secretion were investigated histologically and biochemically. Ambroxol significantly increased the number of active goblet cells in guinea pig tracheal epithelium and total mucopolysaccharide level. Moreover, ambroxol significantly increased the neutral mucopolysaccharide level and PAS-positive substance in the guinea pig tracheal submucosal glands. Ambroxol did not show a significant effect on the content of the total phosphatidylcholine in rat lung lavage fluid, while ambroxol significantly increased the ratio of disaturated phosphatidylcholine to total phosphatidylcholine. From these results, it is suggested that ambroxol increases both the tracheal mucous secretion, especially the neutral mucopolysaccharide, and pulmonary surfactant secretion and these effects reflect part of the expectorant mechanism of the drug.

Ambroxol↗
PubMed2000

Identification of somatotrophs, mammosomatotrophs, and mammotrophs by sandwich cell immunoblot assay in GH-secreting adenomas and prolactinomas: correlations between the proportions of hormone secreting cells and tumor size.

Sandwich cell immunoblot assay(sandwich CIBA) was used to identify somatotrophs (GH cells), mammosomatotrophs, and mammotrophs (PRL cells) in pituitary tumors obtained from patients with GH-secreting adenomas and prolactinomas. The mean serum GH level was 177.6 ng/ml in 19 patients with GH-secreting adenomas and the mean PRL level was 2,129 ng/ml in 9 patients with prolactinomas. GH-secreting adenomas could be divided into 3 groups according to the proportions of the cell types. The GH cell dominant type had more than 70% GH cells. The mammosomatotroph cell dominant type had more than 80% mammosomatotrophs. The non-dominant type had no dominant cell type. There was a good correlation (r2=0.804) between serum GH levels and tumor size in patients with the GH cell dominant type (n=10). The nondominant type (n=8) had a low serum level of GH except for one tumor. The mammosomatotroph cell dominant type (n=1) showed high serum levels of both GH and PRL. All prolactinomas had a predominance of PRL cells. Sandwich CIBA is a simple method for detecting GH cells, mammosomatotrophs, and PRL cells, and useful for classification for GH-secreting adenomas.

Adenoma↗
PubMed2001

Analysis of cortisol secretion in hormonally inactive adrenocortical incidentalomas: study of in vitro steroid secretion and immunohistochemical localization of steroidogenic enzymes.

Adrenal incidentalomas have recently increased in incidence, and thus it has become important to establish clinical management of these patients. It is also important to evaluate whether these tumors are different from preclinical or overt Cushing's syndrome in their steroidogenesis. In this study, we therefore examined steroidogenesis of hormonally inactive adrenal incidentalomas via short-term culture of tumor specimens, in addition to an immunohistochemical study of steroidogenic enzymes. Five patients (two men and three women) diagnosed with adrenocortical incidentaloma without any clinical signs of adrenocortical hormonal excess except for hypertension and disturbed glucose tolerance, were recruited for this study. Hormonal findings, including circadian rhythms for cortisol and ACTH secretion, the response of ACTH to CRH infusion and results of dexamethasone suppression test were all within normal limits in these patients. Immunoreactivity for all steroidogenic enzymes involved in cortisol production was detected in tumor cells in all cases examined. Results of in vitro steroidogenesis analysis using short-term culture revealed that levels of cortisol secretion varied among the cases. There were no differences in the immunolocalization of steroidogenic enzymes and/or the levels of cortisol secretion between these hormonally inactive tumors and preclinical and/or overt Cushing's syndrome. Dehydroepiandrosterone-sulfotransferase (DHEA-ST) immunoreactivity in nonneoplastic regions was suppressed in one case in which the tumor secreted cortisol similar to preclinical and/or overt Cushing's syndrome. These results demonstrate that the levels of in vitro steroid production and/or the immunolocalization of steroidogenic enzymes in hormonally inactive adrenocortical tumors vary markedly and are not overtly different from those of preclinical and/or overt Cushing's syndrome.

17-alpha-Hydroxyprogesterone↗
PubMed1986

Acute effects of GnRF-induced gonadotrophin secretion upon ovarian steroid secretion in the ferret.

The effects of an increase in endogenous gonadotrophin secretion on the production of oestradiol, progesterone, androstenedione and testosterone by the ovaries of anaesthetized anoestrous and oestrous ferrets were followed. Gonadotrophin secretion was enhanced by the injection of gonadotrophin releasing factor (GnRF), and serial blood samples were collected over 9 h for hormone assay. Thyrotrophic hormone releasing factor (TRF) or acetic acid were injected for control purposes. The plasma content of oestradiol in oestrous females was significantly higher than during anoestrus, but secretion of this steroid was not increased by any means. The plasma concentration of progesterone in anoestrous females was significantly higher than during oestrus. It was increased by GnRF in anoestrous ferrets and less markedly in oestrous females. The plasma concentration of androstenedione was raised by GnRF to a greater extent during anoestrus than during oestrus. Testosterone was present in higher concentration in the plasma during anoestrus than during oestrus, and the level was increased by GnRF administration. These findings indicate that the ovaries of the anoestrous ferret secrete significant quantities of steroid hormones, and that they respond readily to gonadotrophic hormone.

Androstenedione↗
PubMed1987

The effect of the somatostatin analog SMS 201-995 on normal growth hormone secretion in the rat. A comparison with the effect of bromocriptine on normal prolactin secretion.

The somatostatin analog SMS 201-995 was recently shown to be effective in suppressing GH secretion and in causing tumour shrinkage in patients with GH-secreting pituitary tumours. In this respect, the action of SMS 201-995 seems similar to that of the dopamine-agonist bromocriptine in patients with PRL-secreting pituitary tumours. In the present study we compared the respective effects of SMS 201-995 and bromocriptine on normal rat GH and PRL release in vivo and in vitro. Both in vitro and in vivo, repeated administration of SMS for up till 6 days suppressed circulating GH concentrations, and the ability of the pituitary glands to release GH in vitro. A dose-dependent diminution occurred of the total pituitary GH content in rats treated in vivo with SMS 201-995 for 4-6 days. During short-term in vitro incubation for only 4 h, the total amount of GH measured in the medium + gland was also diminished. Chronic administration with SMS 201-995 (2 micrograms/kg twice daily for 15 days), however, resulted in a complete desensitization of its inhibitory effect on GH synthesis and release. In similar experiments it was shown that the dopamine agonist bromocriptine affects normal PRL secretion in a different manner. Both in vitro (10 nmol/l) and in vivo administration for 6 days (0.2 mg/kg twice daily) greatly inhibited circulating PRL levels and the ability of the pituitary glands to release PRL in vitro. This is, however, in all instances accompanied by an accumulation of PRL within the pituitary gland.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

Ontogeny of the opioidergic regulation of LH and prolactin secretion in lactating sow. I: failure of naloxone to antagonize suckling-induced changes in LH and prolactin secretion in early lactation, irrespective of pattern of administration.

The principal aim of this study was to investigate the ontogeny of an opioidergic mechanism mediating the suckling-induced inhibition of LH secretion during lactation in sows. In contrast to an increase in LH secretion in response to naloxone treatment on days 10 and 11 of lactation (P < 0.05), a single injection of 2 mg naloxone kg-1 at 39, 51, 63, or 75 h post partum had no effect. However, the last of four injections of 2 mg naloxone kg-1 given at 12 h intervals to group IV sows did elicit a positive LH response (P < 0.05). Multiple injections of 1 mg naloxone kg-1 at 3 h intervals over 30 h on day 10-11 consistently increased (P < 0.05) mean plasma LH with no evidence of induced refractoriness to repeated use of the antagonist. Similarly, naloxone did not affect mean plasma prolactin in the immediate postpartum period, but either repeated naloxone treatments on day 10-11 or single naloxone injections on day 10 or 11 of lactation decreased plasma prolactin (P < 0.05). Therefore, the regulation of LH and prolactin secretion in lactating sows changes with time post partum. An opioid-dependent mechanism is an important component of the suckling-dependent regulation of LH and prolactin secretion in established lactation, but not during the first 72 h postpartum period.

Animals↗
PubMed1991

Increased secretion of insulin-like growth factor-binding proteins and decreased secretion of insulin-like growth factor-II by muscle from growth-retarded neonatal rats.

Insulin-like growth factors (IGFs) and IGF-binding proteins (IGFBPs) may be important factors in the control of neonatal growth. We have examined the production, in vitro, of IGFBPs and IGFs by hind-limb skeletal muscle from normal and small-for-gestational age (SGA) neonatal rats. Conditioned medium was collected from muscle strips after incubation at 37 degrees C for 2 h in Ham's F-12 medium. The conditioned medium was subjected to acid-gel permeation chromatography to separate IGFBPs from IGFs. The binding of 125I-labelled IGF-I to IGFBPs from both control and SGA muscle was displaced equipotently by IGF-I and IGF-II and not at all by insulin. IGFBPs from control and SGA muscles bound IGF-I with comparable affinities (Kd = 0.071 and 0.069 nmol/l respectively). When IGF-II was used as tracer, neither IGF-I nor insulin competed for binding. Western ligand blots of IGFBPs in conditioned media from both control and SGA muscles showed three bands of radioactivity at molecular masses equivalent to 24, 30 and 40 kDa. When the release of IGFBPs by muscle tissue in vitro was quantified by measuring the number of IGF-I binding sites in acid-fractionated medium it was apparent that the muscles from SGA pups secreted significantly more IGFBPs (39.3 +/- 7.5 fmol/mg muscle protein per 2 h) than the muscles from control pups (17.8 +/- 2.7 fmol/mg protein per 2 h; P less than 0.05). In contrast to the IGFBPs, more IGF activity was secreted by the muscles from the control pups (61.1 +/- 15.6 fmol/mg muscle protein per 2 h) than the muscles from the SGA pups (12.6 +/- 5.8 fmol/mg muscle protein per 2 h; P less than 0.05). Analysis of the IGF activity with assays specific for IGF-I and IGF-II showed that both SGA and control muscles secreted predominantly IGF-II with approximately 10% of the total IGF activity measurable as IGF-I. This differential secretion of IGFBPs and IGFs may be associated with the reduced growth potential of the SGA neonate.

Animals↗
PubMed1988

Pancreastatin inhibits insulin secretion and stimulates glucagon secretion in mice.

Recently a new peptide, pancreastatin, was isolated from porcine pancreatic extracts. It contains 49 amino acids and shows a structural similarity to chromogranin A, which occurs in secretory granules of the endocrine pancreas. Furthermore, pancreastatin has been found to inhibit glucose-induced insulin secretion in the perfused rat pancreas. However, its effects under in vivo conditions have never been studied. We have therefore investigated the effects of this peptide on insulin and glucagon secretion in vivo in the mouse. We found that an intravenous injection of pancreastatin (4.0 nmol/kg) lowered basal plasma insulin concentration at 6 min from 55 +/- 8 microU/ml in control mice to 21 +/- 7 microU/ml (P less than .01). The peptide also inhibited the plasma insulin response to both glucose (P less than .01) and the cholinergic agonist carbachol (P less than .001). Furthermore, 2 min after injection of pancreastatin, plasma glucagon concentration had increased to 301 +/- 19 pg/ml compared to 190 +/- 12 pg/ml in control mice (P less than .001). The peptide did not, however, affect the carbachol-induced plasma glucagon response. In addition, pancreastatin induced a transient hyperglycemia. Combined adrenergic blockade by means of a pretreatment of phentolamine and propranolol did not prevent pancreastatin from exerting its effects on plasma insulin levels, whereas the increase in plasma glucagon levels was abolished. Thus, in the mouse, the newly discovered intrapancreatic peptide pancreastatin 1) lowers baseline plasma insulin levels, 2) inhibits glucose- and cholinergically induced insulin secretion, 3) stimulates baseline glucagon secretion, and 4) induces hyperglycemia.

Animals↗
PubMed1977

Gastric acid secretion in patients with symptomatic hiatus hernia and effect of a modified Belsey MK IV repair on gastric acid secretion.

Fasting, basal, and pentagastrin-stimulated (6 microgram/kg body weight) gastric acid secretion was assessed in 53 patients with radiologically verified sliding hiatus hernia without stricture formation. There was no difference in the acid secretory variables between patients with heartburn and those with heartburn and pain. A study of the acid secretory variables in 34 patients before and 3 months after a modified Belsey MK IV repair for symptomatic hiatus hernia showed that after the repair the pH of basal secretion had risen, and that the volume of basal secretion as well as basal and peak acid output had been reduced. These changes must probably be ascribed to an unintentional vagotomy during the operation. It is concluded that in the evaluation of a surgically established barrier against gastro-oesophageal reflux in terms of oesophageal pH, changes in gastric acid secretion should be taken into consideration.

Adult↗
PubMed1982

Calcium and stimulus-secretion coupling in gastric fundic mucosa. Effect of inhibition of calcium transport by verapamil on gastric acid secretion in the isolated guinea pig fundic mucosa and in healthy subjects.

The effect on gastric acid secretion of blocking transmembrane Ca2+ influx into the parietal cells has been studied in the isolated guinea pig fundic mucosa and in healthy volunteers. Verapamil inhibited in a dose-related manner histamine-stimulated acid secretion in the guinea pig mucosa, whereas stimulation with theophylline and dibutyryl cyclic-AMP was unaffected. The effect of verapamil (Isoptin, 2.0 mg/h) on acid secretion stimulated by increasing doses (50, 200, 500 ng/kg-h) of 15-leucine synthetic human gastric I was studied in seven healthy volunteers, alone and in combination with infusion of calcium gluconate (1.0 meq Ca2+/kg-h). Verapamil inhibited the acid response to the lowest dose of gastrin, resulting in a significant increase of D50 of 15-leucine synthetic human gastrin I. This effect was partly reversed by calcium infusion. It is concluded that one of the mechanisms by which extracellular calcium concentration influences acid secretion is by transmembrane influx of Ca2+ during stimulation.

Adult↗