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At least 361 records · Page 20Linked to original sources
PubMed1989

[Tri-annual rhythm of basal acid secretion and secretion stimulated by pentagastrin in duodenal ulcer].

Duodenal ulcer is a recurrent disease with seasonal periodicity for pain and complications such as hemorrhage and perforation. Ulcer craters or symptoms seem to occur preferentially in early spring and autumn. Since acid secretion is one of the pathogenetic factors of the disease, we analyzed retrospectively basal and maximal (pentagastrin) acid secretion data obtained in 341 consecutive patients according to the month in which they were obtained. The patients were classified according to the activity of their ulcer (active, non active) and to the level of the peak acid secretion (hypersecretors, normosecretors). Basal acid concentration and output, and peak acid output were, both overall and month by month, higher in patients with active duodenal ulcer disease than in those who were non active, and in hypersecretors than in normosecretors. For all 341 patients as well as for normosecretors and non active ulcer patients, a triannual rhythm was detected for stimulated acid concentration and peak acid output. The highest values were noted in February, June, and October (period: 4 months). The amplitude of these rhythms was 3 to 4 percent, with differences between highest and lowest values of 30.4 mmol/l for concentration and 17.1 mmol/h for peak acid output. These rhythms for acid secretion during the year may contribute to the periodicity of duodenal ulcer events and should be analyzed in association with other factors which could be implied in ulcerogenesis. Moreover, this seasonal periodicity of acid secretion in duodenal ulcer should be taken into account in all therapeutic trials in which acid secretion is analyzed.

Adolescent↗
PubMed1987

Evaluation of esaprazole activity on basal gastric secretion and on pentagastrin-stimulated secretion in healthy volunteers.

The antisecretory effects of esaprazole on basal gastric secretion and on pentagastrin-stimulated secretion (6 micrograms/kg subcutaneously) were evaluated in two trials carried out on 19 healthy volunteers. All trials were carried out according to a randomized double-blind crossover design versus a placebo. The oral administration of 900 mg of esaprazole 30 min before starting the secretion test, induced a certain reduction of all the gastric secretion parameters. The reduction of both basal and stimulated secretion was significantly (p less than 0.001) more evident after the oral administration (gastric instillation) of 1800 mg of the drug 60 min before starting the study. Esaprazole was shown to have a dose-dependent antisecretory activity which was particularly evident on secretion volume and acid output.

Adult↗
PubMedDate not supplied

[Secretion of pancreatic polypeptide in cats in response to different stimuli; correlation with gastric acid secretion].

The pancreatic polypeptide response to a meal depends on various mechanisms, which are only partly understood. The aim of this study was to define whether humoral factors and nutrients which modulate postprandial gastric acid secretion play a role in the regulation of pancreatic polypeptide secretion. Our study was performed in the cat, a species in which pancreatic polypeptide release has never been explored. The animals were provided with a gastric fistula and a Heidenhain pouch and received, in a random order, mixed liver (50 g) per os or different nutriments which were introduced directly into the gastric fistula in identical final volumes: 50 g mixed liver; 1.5 to 12 g oligopeptides; or 2 g of triglycerides or glycogen. Acid output and pancreatic polypeptide secretion were measured over 150 min. In the cat as in dog and man, a mixed meal induced a five to ten-fold increase of plasma pancreatic polypeptide. The protein fraction of the meal was the most potent stimulus for release of this peptide and the pancreatic polypeptide response to protein seemed to be dose-related. The lipid and carbohydrate components of the meal were only weak stimulants. In the cat, a central vagal stimulation is effective on pancreatic polypeptide release, as on gastric acid secretion, since 2-deoxyglucose stimulated both secretions (about 15 p. 100 of maximal response to a meal). The integrated pancreatic polypeptide release and the Heidenhain pouch acid secretion in response to nutriments were correlated during the 30-120 min period.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Vitamin A stimulation of insulin secretion: effects on transglutaminase mRNA and activity using rat islets and insulin-secreting cells.

Retinol or retinoic acid is required for insulin release. Retinoids increase transglutaminase activity, and transglutaminase has been implicated in islet insulin release. To examine whether transglutaminase could mediate effects of retinoids on insulin secretion, we measured (i) transglutaminase activity in islets from rats deficient in vitamin A or repleted with retinol or retinoic acid, (ii) transglutaminase activity in RINm5F and INS-1 insulin-secreting cells cultured in retinol or retinoic acid, (iii) mRNA for transglutaminase in RINm5F and INS-1 cells, and (iv) insulin secretion from INS-1 cells in response to retinoic acid. Islets from rats repleted with retinol or retinoic acid showed more than twice the transglutaminase activity of islets from vitamin A deficient rats. Retinoic acid increased RINm5F cells and INS-1 cell transglutaminase activity. Retinol did not increase transglutaminase activity. Transglutaminase mRNA was detected in INS-1 cells but not in RINm5F cells. Retinoic acid increased insulin secretion from INS-1 cells as observed previously in RINm5F cells. In conclusion, retinoic acid increases transglutaminase activity in both rat islets and two insulin-secreting from INS-1 cells. Transglutaminase is a candidate for mediating retinoid-induced changes in insulin secretion.

Animals↗
PubMed1998

Effects of acid-degraded products of leminoprazole on acid secretion, mucus secretion and synthesis, and indomethacin-induced damage in cell culture.

We examined the effects of four acid-degraded products of leminoprazole on [1] acid secretion by parietal cells, [2] mucus secretion and synthesis by epithelial cells and [3] indomethacin-induced damage to epithelial cells. These gastric cells were prepared from rabbit stomachs. Upon stimulation with 10 microM histamine, acid secretion by parietal cells was inhibited by leminoprazole, sulfide and 2-(isobutylmethylamino)benzylalcohol. Sulfide also inhibited dibutyryl cyclicAMP (100 microM)-stimulated secretion. However, the inhibitory effects of such compounds were observed only at high concentrations, in comparison with the antisecretory concentrations of leminoprazole. On the other hand, among acid-degraded products, only sulfide enhanced mucus secretion and synthesis by epithelial cells. The stimulatory effects of sulfide were the same as those of leminoprazole. Furthermore, the effects of sulfide as well as leminoprazole were suppressed by NG-nitro-L-arginine methyl ester (L-NAME), and L-arginine, not D-arginine, prevented the inhibition by L-NAME. In contrast, all degraded products failed to protect epithelial cells against indomethacin-induced damage. Overall, these results suggest that only the mucus-elevating effect of administered leminoprazole may be partly due to the stimulatory effects of sulfide derived from leminoprazole on mucus secretion and synthesis by epithelial cells.

Acids↗
PubMed2003

Mechanisms of exocytosis in insulin-secreting B-cells and glucagon-secreting A-cells.

In pancreatic B- and A-cells, metabolic stimuli regulate biochemical and electrical processes that culminate in Ca2+-influx and release of insulin or glucagon, respectively. Like in other (neuro)endocrine cells, Ca2+-influx triggers the rapid exocytosis of hormone-containing secretory granules. Only a small fraction of granules (<1% in insulin-secreting B-cells) can be released immediately, while the remainder requires translocation to the plasma membrane and further "priming" for release by several ATP- and Ca2+-dependent reactions. Such functional organization may account for systemic features such as the biphasic time course of glucose-stimulated insulin secretion. Since this release pattern is altered in type-2 diabetes mellitus, it is conceivable that disturbances in the exocytotic machinery underlie the disease. Here I will review recent data from our laboratory relevant for the understanding of these processes in insulin-secreting B-cells and glucagon-secreting A-cells and for the identification of novel targets for antidiabetic drug action. Two aspects are discussed in detail: 1) The importance of a tight interaction between L-type Ca2+-channels and the exocytotic machinery for efficient secretion; and 2) the role of intragranular acidification for the priming of secretory granules and its regulation by a granular 65-kDa sulfonylurea-binding protein.

Adenosine Triphosphate↗
PubMed2005

Mechanism of D(2) agonist-induced inhibition of GH secretion from human GH-secreting adenoma cells.

The mechanism of dopamine D(2) agonist-induced inhibition of GH secretion from GH-secreting adenoma cells was investigated by measurement of intracellular calcium concentration ([Ca(2+)] (i)) and static incubation experiment. Bromocriptine decreased [Ca(2+)](i) in a concentration-dependent manner through D(2) receptor. The inhibition was abolished by pertussis toxin pretreatment. Bromocriptine did not decrease [Ca (2+)](i) after nitrendipine had decreased it. 8Br-cAMP increased [Ca(2+)](i) but application of bromocriptine decreased it, suggesting that bromocriptine-induced inhibition of [Ca(2+)](i) is not dependent on bromocriptine-induced inhibition of adenylyl cyclase. Static incubation experiment revealed that bromocriptine inhibited GH secretion in a concentration-dependent manner. The inhibition was through D(2) receptor and was abolished by pertussis toxin pretreatment. 8Br-cAMP increased GH secretion. Bromocriptine decreased GH secretion even after 8Br-cAMP pretreatment. However, the GH release from cells incubated with bromocriptine alone was significantly less than that from cells incubated with bromocriptine after 8Br-cAMP pretreatment, suggesting a modulatory action of cAMP system in bromocriptine response.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1995

Inhibition of angiotensin II- and potassium-mediated aldosterone secretion by KN-62 suggests involvement of Ca(2+)-calmodulin dependent protein kinase II in aldosterone secretion.

Calcium is now acknowledged to play a major role as a cellular mediator of aldosterone secretion. However, the intricacies of the involvement of calcium in aldosterone secretion have not been clearly defined. We have shown here that calmodulin-dependent kinase II is involved in angiotensin II- and potassium-evoked aldosterone secretion as judged by the marked inhibitory effect of KN-62, a specific inhibitor of such a kinase, on aldosterone secretion and this inhibition was similar to that produced by calmodulin inhibitor, W-7. These results further strengthen the case for the participatory role of calcium-calmodulin system in aldosterone secretion.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1997

Insulin secretagogues with an imidazoline structure inhibit arginine-induced secretion from isolated glucagon secretion from isolated rat islets of Langerhans.

It is well documented that imidazoline compounds such as efaroxan and phentolamine act as potent insulin secretagogues both in vivo and in vitro, an effect which is mediated principally by blockade of ATP-sensitive potassium channels in the pancreatic B-cell. However, little is known about the effects of these drugs on the secretion of other pancreatic hormones and, in the present work, we have investigated the effects of selective imidazoline compounds on glucagon release from isolated rat islets of Langerhans. None of several imidazoline compounds tested (efaroxan, phentolamine, idazoxan, antazoline) affected glucagon secretion from islets incubated with 4 mM glucose. However, when the rate of glucagon release was stimulated by L-arginine (20 mM) efaroxan caused a rapid, sustained and dose-dependent inhibition of the secretory response (EC50 approximately 30 microM). This effect was seen under both static incubation and islet perifusion conditions. Antazoline and phentolamine also inhibited arginine-induced glucagon secretion, whereas idazoxan (an imidazoline which does not affect insulin secretion) failed to alter glucagon release. The inhibitory effects of imidazolines on glucagon release were not secondary to changes in insulin secretion. Taken together, the results indicate that pancreatic A-cells express functional imidazoline receptors which can regulate the secretory activity of the cells.

Animals↗
PubMed1992

Cloning, nucleotide sequence and characterization of the gene encoding the Erwinia chrysanthemi B374 PrtA metalloprotease: a third metalloprotease secreted via a C-terminal secretion signal.

Erwinia chrysanthemi, a phytopathogenic enterobacterium, secretes three proteases (PrtA, PrtB and PrtC) into the extracellular medium. The gene encoding the 50 kDa protease, prtA, was subcloned from a recombinant cosmid carrying a fragment of the E. chrysanthemi B374 chromosome. prtA was shown to be located immediately 3' to the structural genes for the other two extracellular proteases. The amino acid sequence of PrtA, as predicted from the prtA nucleotide sequence, showed a high level of homology with a family of metalloproteases that are all secreted via a signal peptide-independent pathway, including PrtB and PrtC of E. chrysanthemi B374, PrtC of E. chrysanthemi EC16, PrtSM of Serratia marcescens and AprA of Pseudomonas aeruginosa. PrtA secretion requires the E. chrysanthemi protease secretion factors PrtD, PrtE and PrtF. The secretion signal of PrtA is near to the carboxy-terminal end of the protein, as was previously shown to be the case for PrtB and PrtSM and for Escherichia coli alpha-hemolysin. The C-termini of these four proteins do not show extensive primary sequence homology, but PrtA, PrtB and PrtSM each have a potential amphipathic alpha-helix located close to the C-terminus.

Amino Acid Sequence↗
PubMed1993

Functional analysis of the Lactococcus lactis usp45 secretion signal in the secretion of a homologous proteinase and a heterologous alpha-amylase.

The ups45 gene encodes the major extracellular protein from Lactococcus lactis. The deduced sequence of the 27 residue leader peptide revealed the tripartite characteristics of a signal peptide. This leader peptide directed the efficient secretion of the homologous proteinase (PrtP) in L. lactis, indicating that the putative signal peptide of PrtP can be replaced by the 27 residue Usp45 leader peptide. In addition, the 27 residue leader peptide could be used to secrete the Bacillus stearothermophilus alpha-amylase, encoded by the amyS gene. Fusion of the usp45 promoter region and various parts of the leader sequence to an amyS gene devoid of its signal sequence, showed that in Escherichia coli the first 19, 20, and 27 residues of the Usp45 leader are able to direct alpha-amylase secretion. In L. lactis the shorter signal peptides did not result in secretion of alpha-amylase, providing experimental evidence for the hypothesis that gram-positive bacteria require a longer signal peptide for secretion than gram-negative organisms.

Amino Acid Sequence↗
PubMed1976

Comprehensive formal models for pancreatic calcium secretion. With reference to "exchange-diffusion," "two-component," and "unicellular" models of electrolyte secretion.

This is a theoretical paper in which comprehensive formal models are developed for all possible modes of entry of calcium into pancreatic juice. The 15 models include entry via: (1) the chloride-rich secretion, (2) the bicarbonate-rich secretion, (3) protein-bound calcium, and (4) interstitial fluid (ISF), plus the various possible combinations of these. Equations are presented for both calcium-volume and calcium-bicarbonate relationships. Each equation is modified as necessary to conform to the three current models for sodium, chloride, and bicarbonate secretion: (1) "exchange-diffusion," (2) "two-component," and (3) "unicellular" models. We believe the models provide a sound theoretical framework on which to build an understanding of pancreatic calcium secretion. Subsequent papers will be concerned with the physicochemical state of calcium in the juice, the relative contribution of ISF, and the development of an overall model for pancreatic calcium secretion. The long-term objective is to provide a rational approach for the understanding of pancreatic calcification and stone formation.

Bicarbonates↗
PubMed1986

Effect of ethanol ingestion on postprandial gastric emptying and secretion, biliopancreatic secretions, and duodenal absorption in man.

Although abdominal complaints are frequent in both acute and chronic alcoholism, little is known of the effect of ingestion of ethanol with a meal on the function of the upper digestive tract. We have studied the effects of oral ethanol (1 g/kg body wt) taken with food on the gastric emptying rate of a solid-liquid meal as measured by a dual radioisotope technique in six normal subjects; and the gastric response (emptying and secretion), biliopancreatic secretions, and duodenal nutrient absorption after an homogenized meal, as evaluated by a gastroduodenal intubation-marker perfusion technique on seven healthy volunteers. In the latter experiments, radioimmunoassays of gastrin, secretin, cholecystokinin, pancreatic polypeptide, motilin, somatostatin, gastric inhibitory polypeptide, and vasoactive intestinal polypeptide were performed serially. As compared with the control experiment, alcohol induced the following effects: marked delay of gastric emptying of solids, smaller slowing effect on gastric emptying of the liquid phase of the solid-liquid meal and of the homogenized meal; no significant change in gastric acid secretion; no change in the overall postprandial pancreatic enzyme outputs, but a delay of lipase secretion; no change in the early bile salt postprandial output, but a reduced bile salt secretion from the second postprandial hour onwards; no significant change in carbohydrate and lipid duodenal absorption; and a significantly greater postcibal gastrin release. The mechanisms for these effects of alcohol on upper digestive tract function remain to be clarified.

Adult↗
PubMed1987

Regulation of exocytosis in electrically permeabilized insulin-secreting cells. Evidence for Ca2+ dependent and independent secretion.

The regulation of insulin secretion from RINm5F cells exposed to high voltage discharge has been investigated. Electron microscopy revealed that the overall structure of the cells was preserved after permeabilization. In this preparation insulin release was stimulated by Ca2+ (EC50 = 2.4 microM). The stable GTP analogue GTP gamma S enhanced secretion both at intermediate (nano- to micromolar) and vanishingly low (less than 10 pM) Ca2+ concentrations. At optimal Ca2+ (10 microM) the effect of GTP gamma S was greatly reduced. We investigated whether the secretory response to GTP analogues was mediated by any of three enzyme systems regulated by GTP-binding proteins, i.e. generation of cyclic AMP by adenylate cyclase, of diacylglycerol by phospholipase C and of arachidonic acid by phospholipase A2. The involvement of these messenger systems could be excluded as (i) cyclic AMP only had minor, Ca2+ dependent effects, (ii) phospholipase C was not activated in the absence of Ca2+ and insulin secretion due to the phorbol ester TPA displayed a different Ca2+ dependency, (iii) arachidonic acid did not elicit Ca2+ independent insulin secretion. These results, taken together with the finding that insulin secretion due to Ca2+ or TPA is attenuated by the inhibitory guanine nucleotide GDP beta S, suggest the existence of a regulatory site in exocytosis which is sensitive to guanine nucleotides.

Animals↗
PubMed1984

Chloride secretion by canine tracheal epithelium: IV. Basolateral membrane K permeability parallels secretion rate.

We evaluated the K conductance properties of the basolateral membranes of the surface cells of canine tracheal epithelium using microelectrode techniques. Studies were conducted under basal conditions (indomethacin, 10(-6) M, mucosal solution) and after stimulation of electrogenic Cl secretion with epinephrine (10(-6) M, serosal solution). Elevated serosal solution [K] depolarized the electrical potential differences across the apical (psi a) and basolateral (psi b) membranes in both the presence and absence of epinephrine. Serosal barium (0.5 mM) also depolarized psi a and psi b and selectively increased basolateral membrane resistance threefold. We also used K-selective microelectrodes to determine cell K activity (acK) and the driving force for K transport across the limiting membranes under basal and stimulated conditions. Stimulation of Cl secretion was not associated with significant changes in psi b or acK so that the driving force for K exit from cell to serosal solution (ca. 20 mV) was not altered. There was close agreement between the basolateral membrane electromotive force (Eb) determined from prior studies (M.J. Welsh, P.L. Smith and R.A. Frizzell, J. Membrane Biol. 71:209-218, 1983) and the chemical potential difference for K across this barrier (EbK) in the presence and absence of epinephrine. These findings support the notion that the basolateral membrane is characterized by a high conductance to K under both secreting and nonsecreting conditions and indicate that the decrease in basolateral membrane resistance that accompanies stimulation of Cl secretion results from an increase in its K conductance. This obviates changes in acK that would otherwise accompany increased Na/K pump activity and, by hyperpolarizing psi a, establishes the electrical driving force for Cl secretion across the apical membrane.

Animals↗
PubMed1998

Reliable gastric tonometry after coronary artery surgery: need for acid secretion suppression despite transient failure of acid secretion.

OBJECTIVE: To study the need for suppression of gastric acid secretion for reliable intragastric partial pressure of carbon dioxide (PCO2) tonometry by evaluating the effect of an oral dose of sodium bicarbonate before and after administration of the H2-blocker ranitidine to mimic CO2 generation following the buffering of acid by bicarbonate in patients after cardiac surgery. DESIGN: Prospective, open, non-randomized clinical study. SETTING: Cardiothoracic intensive care unit at a university hospital. PATIENTS: 10 patients after elective coronary artery bypass surgery. INTERVENTIONS: An oral dose of 500 mg sodium bicarbonate before and after acid secretion suppression by 100 mg ranitidine as an intravenous bolus given at approximately 3 h after surgery (day 0) and on the first postoperative day (day 1). MEASUREMENTS AND RESULTS: Intragastric PCO2 (iPCO2; tonometry), gastric juice pH (aspirate) and arterial blood gas values were measured. On day 0, the iPCO2 was 25 +/- 5 mmHg before and 31 +/- 5 mmHg after the bicarbonate dose, 29 +/- 5 mmHg after ranitidine infusion, and 31 +/- 5 mmHg after the bicarbonate dose following the ranitidine infusion (NS). On day 1, the basal iPCO2 was 32 +/- 4 mmHg and it increased to 56 +/- 25 mmHg following bicarbonate (p < 0.01). After ranitidine, the iPCO2 was 33 +/- 4 mmHg before and 40 +/- 14 mmHg after bicarbonate (NS). Basal gastric juice pH was > 4 in nine of ten patients on day 0 and > 4 in seven of ten patients on day 1. CONCLUSIONS: Pharmacological suppression of gastric acid secretion is mandatory for reliable iPCO2 tonometry after cardiopulmonary bypass surgery, even when gastric acid secretion is transiently inhibited. In fact, gastric acid secretion was inhibited immediately after surgery, but returned on the first postoperative day in most patients, as judged from the bicarbonate back titration of gastric acid, even when gastric juice pH was relatively high.

Administration, Oral↗
PubMed2001

Dynamics of protein and fluid secretion from the major salivary glands of rat: relevance of research findings to clinically observed defective secretion in cystic fibrosis.

Although there are indications of a defect in secretion of protein from exocrine cells in cystic fibrosis (CF), this remains an aspect of CF research that has not been adequately addressed. Using salivary glands of rat as model systems, and following the effects of parasympathetic and sympathetic autonomic nerve stimulation on these glands, we demonstrate the existence of three separate pathways through which secretion of protein can be evoked from serous and mucous exocrine cells. These pathways allow the secretion of proteins from the intracellular compartments in a constitutive, intermediate or regulated manner. The primary aspects of secretory profile including concentration and the degree of hydration of secreted material differ greatly between the pathways, are cell type specific, and presumably are a direct consequence of controlled changes in the levels of second messengers induced upon stimulation of these cells. As previously published reports suggest that only the beta-adrenergic regulated pathway is affected by CF, differences between the pathways in their secretory profiles may influence the development of lung disease, through disparate disturbances in the secretion of protein and fluid from serous and mucous cells of the submucosal glands that line the bronchiolar tree in humans. We gratefully acknowledge support from The Wellcome Trust and from The European Union Biomed II Programme.

Amylases↗
PubMed2005

Polarization and secretion of cathepsin K precede tartrate-resistant acid phosphatase secretion to the ruffled border area during the activation of matrix-resorbing clasts.

The activation sequence of clasts (the designation clast was used because ultrastructurally in this tissue, it is not always possible to differentiate between chondroclasts sitting on cartilage and osteoclasts sitting on bone matrix) was studied in vivo using the healing of low-phosphate, vitamin D-deficiency rickets as a model system. Thus, the bones of 7-week-old rachitic animals were analyzed with a combination of morphological, biochemical, and molecular biological methods at 48 and 72 h, respectively, after change to normal food. A quantitative ultrastructural analysis showed that the number of clast profiles exhibiting the characteristic polarized features of actively resorbing cells, i.e., ruffled borders and clear zones, had reached normal levels after 48 h. By combining the data with quantitative analyses by the immunogold technique, we demonstrated that cathepsin K secretion was coupled to ruffled border formation in clasts irrespective of whether the number of polarized clasts was low (in rickets) or high (in healing). In contrast, the levels of tartrate-resistant acid phosphatase (TRAP) both between ruffles and in the outside matrix adjoining the ruffled border were low in polarized clasts both in rickets and at the early (48 h) healing time-point, but were increased at the latest (72 h) healing time-point. Interestingly, expression of TRAP and the cathepsin K at the mRNA level, as well as protein expression and the activity of TRAP, were not different during the healing sequence. Although the two enzymes are confined to the same clast populations, their secretion during the resorption process is apparently differentially regulated: cathepsin K secretion is coupled to ruffled border formation in clasts, whereas TRAP is secreted at a later stage during the resorption sequence, suggesting a role for secreted TRAP as a modulator of resorptive activity.

Acid Phosphatase↗