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PubMed2004

Regulation of apical surface fluid and protein secretion in human airway epithelial cell line Calu-3.

We evaluated the relationship between apical surface fluid (ASF) and protein secretion in Calu-3 cells grown at an air-liquid interface. Calu-3 monolayers responded to forskolin, a cystic fibrosis transmembrane regulator (CFTR) channel agonist, by secreting a significant amount of ASF. Such a response from Calu-3 monolayers was not observed with CFTR channel blockers glybenclamide and DPC. Other ion channel mediators, PGF-2alpha, PMA, DNDS, and DIDS, had no effect on Calu-3 ASF secretion. Forskolin decreased Calu-3 protein secretion and glybenclamide increased protein secretion. Similarly, forskolin decreased Calu-3 lysozyme secretion, whereas glybenclamide and DPC increased lysozyme secretion. We observed significant changes in Calu-3 fluid and protein secretions with ion channel mediators known to alter CFTR activity. Our results demonstrate a functional link between fluid and protein secretions in Calu-3 apical surface and suggested a possible involvement of CFTR in these processes.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1982

Crypts are the site of intestinal fluid and electrolyte secretion.

The site of adenosine 3',5'-monophosphate-mediated fluid and electrolyte secretion across mammalian large intestine was found to be the crypts of Lieberkühn by means of two techniques. First, the formation of fluid droplets was visualized on the oil-covered mucosal surface directly over crypt duct openings when secretion was stimulated. Second, microelectrode impalement of individual surface and crypt cells revealed that only crypts cells produced a pattern of secretagogue induced alterations in membrane potential and resistance that was characteristic of secretory epithelia.

Amiloride↗
PubMed1997

Na(+)-dependent and -independent Cl-/HCO-3 exchange mediate cellular HCO3- transport in cultured human intrahepatic bile duct cells.

Biliary epithelial cells (cholangiocytes) modulate bile fluidity and alkalinity absorbing and/or secreting fluid and electrolytes, particularly HCO3- and Cl-. Mechanisms responsible for transepithelial H+/HCO3- secretion in human cholangiocytes are largely unknown. Human cholangiocytes isolated by enzymatic digestion and immunomagnetic purification from normal liver tissue obtained from reduced grafts used for pediatric liver transplantation were cultured in the presence of human hepatocyte growth factor. Maintenance of cholangiocyte phenotypic features was assessed using markers such as cytokeratin 19, gamma-glutamyltranspeptidase, vimentin, factor VIII-related antigen, desmin, epithelial membrane antigen (EMA), and human epithelial antigen (HEA) 125. Intracellular pH (pHi) transients were measured microfluorimetrically 2'7'-Bis(2-carboxyethyl)-5,6, carboxyfluorescein-acetossimethylester (BCECF). In the absence of HCO3-, pHi recovery from an intracellular acid load (ammonia pre-pulse technique) was Na(+)-dependent and amiloride-inhibitable. No Na(+)-independent recovery was recorded even after stimulation with agents raising intracellular cyclic adenosine monophosphate (cAMP) concentrations. In the presence of HCO3-, recovery from an intracellular acid load required Na+, but was only partly inhibited by amiloride. In these conditions H+ extrusion was inhibited by 4,4-diisothiocyan atostilben-2,2-disulfonic acid (DIDS) and by intracellular Cl- depletion. Acute removal of extracellular Cl induced a pHi alkalinization that was inhibited by DIDS. pHi recovery from an intracellular alkaline load (isohydric CO2 changes) was Cl(-)-dependent and DIDS-inhibitable. Administration of agents raising intracellular cAMP concentrations increased both Na(+)-dependent and Na(+)-independent Cl-/HCO-3 exchange activity. Stimulation of Cl-/HCO3- exchange activity was not prevented by the Cl- channel inhibitor 5'-nitro-2(2)-phenylpropyl-amino-benzoate(NPPB). In conclusion, human cholangiocytes possess two acid extruders (Na+/H+exchanger and Na(+)-dependent Cl-/HCO3- exchange) and an acid loader (Cl-/HCO3- exchange), whereas no evidence was found for cAMP activated H(+)-ATPase. Bicarbonate influx is thus mainly mediated by Na-dependent Cl-/HCO3- exchange, whereas Na+:HCO-3 cotransport is not active in the physiological range of pHi. Stimulation of Na(+)-independent Cl-/HCO3- exchanger by cAMP does not require activation of Cl- conductances. These mechanisms may underlay hormone-regulated biliary HCO3- secretion in the human biliary tree.

Antiporters↗
PubMed1998

The polarity of choroid plexus epithelial cells in vitro is improved in serum-free medium.

The influence of culture conditions on the development of normal characteristics of the choroid plexus epithelium has been investigated in vitro with respect to polarity, barrier properties, transport, and secretory activity. Withdrawal of serum supplement in the culture medium of cells grown on filters caused morphologically visible changes by an increased trimming of microvilli at the apical membrane side, which is accompanied by an increased expression of the Na+,K+-ATPase. Moreover cells under serum-free conditions exhibit structural changes in tight junctional zonula occludens protein-1 (ZO-1) organization, a reduced permeability, and a drastically increased electrical resistance from 150 ohms x cm2 in the presence of serum to 1,500 ohms x cm2 after serum withdrawal. Under these conditions, cell monolayers are able to build up a transcellular proton gradient and to secrete fluid into the upper (apical) filter compartment, which is accompanied by a polarized secretion of proteins like transthyretin. Active transport of the dyes fluorescein and phenol red by the organic anion transporter is found to be driven by the Na+,K+-ATPase. We come to the conclusion that removal of serum favors the differentiation process of the plexus epithelium in vitro, which brings the cell culture model closer to the physiological situation in vivo. We present preliminary evidence that epidermal growth factor may be one component in serum preventing the proper in vitro differentiation.

Animals↗
PubMed1982

Migrating action-potential complex activity in absence of fluid production is produced by B subunit of cholera enterotoxin.

The myoelectric response and fluid output from in vivo rabbit ileal loops injected with B subunits of purified cholera enterotoxin are compared with the response to the purified cholera holotoxin. Migrating action-potential complex (MAPC) frequency is similar after injection of purified cholera toxin or B subunits. In contrast, fluid output after B-subunit injection is significantly (P less than 0.05) less than fluid output after purified cholera toxin injection. Specific antiserum to the holotoxin incubated with holotoxin at equivalence significantly decreased both MAPC activity (P less than 0.05) and fluid output (P less than 0.001) from the purified toxin. Purified cholera toxin and B subunits, modified by reaction with 2-nitrophenylsulfonyl chloride to produce monomeric B fractions with decreased GM1 ganglioside-binding properties, produced significantly (P less than 0.05) less fluid output and MAPC activity. Binding of the toxin or B subunits in the aggregated form is essential for the expression of MAPC activity or fluid output. These results suggest that the B subunit of cholera toxin produces MAPC activity in the rabbit ileum in the absence of fluid production. Furthermore, previous assumptions that MAPC activity is linked to fluid secretion should be reconsidered. It appears that the gut responses to cholera toxin, fluid production, or MAPC activity are produced by separate mechanisms.

Action Potentials↗
PubMed1987

Nerve interactions in salivary glands.

In the salivary reflex, not only secretory cells are activated, but also myo-epithelial cells are contracted to support these cells and promote the flow of saliva, and blood vessels dilate to meet the increased demands of the tissues. The various effector cells often receive nerves from both parts of the autonomic system, and interactions may occur when the nerves act on the same type of effector, or on different types of effectors. While in an experiment electrical stimulation of the sympathetic trunk may decrease a parasympathetic salivary flow by causing marked vasoconstriction, this does not occur in the salivary reflex, since the vasoconstrictors do not take part. On the contrary, the normal sympathetic vasoconstrictor tone of the resting gland is easily overcome by activity in parasympathetic vasodilator nerves when secretion starts. Pronounced synergism can be demonstrated between sympathetic and parasympathetic secretory nerves. In dogs, for instance, in which sympathetic secretion is beta-adrenoceptor-mediated, this is marked in the case of fluid secretion. In rats and rabbits, in which beta-receptors elicit secretion of amylase, the potentiating interaction among the nerves is striking when amylase secretion is considered. Even the random release of acetylcholine from the post-ganglionic parasympathetic axons, by itself insufficient to evoke secretion, can increase the sympathetic effects. Motor nerves interact with secretory nerves by causing myo-epithelial contraction, mechanically promoting secretion. Interactions between the nerves in their long-term regulatory function on the sensitivity of the acinar secretory and myo-epithelial cells can also be demonstrated.

Animals↗
PubMed1976

Active transport of sodium by the malpighian tubules of the tsetse fly Glossian morsitans.

Isolated Malpighian tubules of Glossina morsitans are able to transport sodium against its concentration gradient. Their rate of secretion is dependent on the sodium concentration of the bathing medium. Potassium must be present in the bathing solution for rapid secretion to be maintained, but it does not play an active role in fluid secretion. Lithium and ammonium ions are able to substitute partially for sodium, other monovalent cations cannot. Ouabain does not affect rapid secretion by Glossina tubules in vitro. Conclusions drawn from the results are incorporated into a model of Malpighian tubule cell function in this insect.

Animals↗
PubMed1980

Active chloride secretion in the normal human jejunum.

To determine whether the small intestine normally secretes fluid, it would be necessary to reduce or inhibit the greater absorptive processes that would otherwise mask such secretion if present. To do this, we perfused bicarbonate-free solutions in the jejunum of normal subjects, because it has been shown that active absorption from this part of the human small intestine is dependent on luminal bicarbonate. We found that the jejunum did secrete sodium chloride and water when isotonic bicarbonate-free solutions were perfused. Further studies revealed that the sodium secretion was passive, but that chloride was secreted against an electrochemical gradient and that observed chloride flux ratios did not agree with the flux ratios calculated for passive chloride movement. We conclude, therefore, that the normal jejunum actively secretes chloride, but that this is masked by greater absorptive processes when balanced electrolyte solutions are perfused. The rate of this active chloride secretion may be one of the factors that regulate the rate of fluid absorption in the normal human intestine.

Bicarbonates↗
PubMed1975

Methylxanthine induced small intestinal secretion.

Methylxanthines, being potent phosphodiesterase inhibitors, produce increased intestinal cyclic AMP levels and would be predicted to produce increased net intestinal fluid secretion. Their effect when presented to the intestinal lumen, which would be analogous to human ingestion, had not been previously determined. Isolated loops of rat jejunum were perfused with solutions of caffeine and theophylline in vivo. There was a decrease in net fluid absorption in both neonatal and mature animals exposed to theophylline. Mature animals exposed to caffeine developed a prompt secretory response, comparable to thax induced by cholera toxin. The data indicate that methylxanthines are potent intestinal secretagogues when administered intraluminally and suggest that secretory stimulation could be important in the gastrointestinal symptomatology elicited in man by these compounds.

Animals↗
PubMed2000

Role of the enteric nervous system in the fluid and electrolyte secretion of rotavirus diarrhea.

The mechanism underlying the intestinal fluid loss in rotavirus diarrhea, which often afflicts children in developing countries, is not known. One hypothesis is that the rotavirus evokes intestinal fluid and electrolyte secretion by activation of the nervous system in the intestinal wall, the enteric nervous system (ENS). Four different drugs that inhibit ENS functions were used to obtain experimental evidence for this hypothesis in mice in vitro and in vivo. The involvement of the ENS in rotavirus diarrhea indicates potential sites of action for drugs in the treatment of the disease.

Animals↗
PubMed1999

Substance P inhibits pancreatic exocrine secretion via a neural mechanism.

We investigated the effects of the sensory neuropeptide substance P (SP) on amylase and fluid secretion in the isolated vascularly perfused rat pancreas. SP inhibited CCK-induced amylase release and secretin-induced juice flow via the pancreatic duct in a dose-related fashion. Threshold inhibition occurred following addition of 10(-10) M SP to the perfusate, and maximal inhibition was seen with 10(-8) M SP. The effects of SP were partially blocked by both the neurokinin-1 (NK1) and neurokinin-2 (NK2) receptor antagonists. Atropine and TTX blocked SP-induced effects on both amylase secretion (26 and 63% blockade, respectively) and pancreatic juice flow (21 and 79% blockade, respectively). Excitation of pancreatic sensory nerves using capsaicin (in the absence of SP) inhibited both amylase and pancreatic juice flow via activation of the NK1 receptor. We conclude that SP inhibits exocrine secretion via an indirect neural mechanism.

Animals↗
PubMed1995

Role of 5-hydroxytryptamine type 3 receptors in rat intestinal fluid and electrolyte secretion induced by cholera and Escherichia coli enterotoxins.

Cholera toxin and Escherichia coli heat labile toxin (LT) induced intestinal secretion has in the past been attributed exclusively to an increase in intracellular cAMP whereas E coli heat stable toxin (ST) induced secretion is mediated through cGMP. Evidence is accumulating on the importance of 5-hydroxytryptamine (5-HT) in cholera toxin induced secretion, but its role in LT and ST is not well established. This study therefore investigated in vivo the effect of 5-HT3 receptor antagonist, granisetron, on intestinal fluid and electrolyte secretion induced by cholera toxin, LT, and ST. Granisetron (30, 75, 150, or 300 micrograms/kg) was given subcutaneously to adult male Wistar rats 90 minutes before instillation of 75 micrograms cholera toxin or 50 micrograms LT in isolated whole small intestine. In situ small intestinal perfusion was performed with an iso-osmotic plasma electrolyte solution (PES) to assess fluid movement. In a second group of animals, granisetron (300 micrograms/kg) was given subcutaneously and two hours later small intestinal perfusion with PES containing 200 micrograms/l ST was performed. Cholera toxin induced net fluid secretion (median -50.1 microliters/min/g (interquartile range -59.5 to -29.8)) was found to be dose dependently decreased or abolished by granisetron (plateau effect at 75 micrograms/kg: 18 (-7.8 to 28), p < 0.01). Granisetron in high dose (300 micrograms/kg), however, failed to prevent LT or ST induced secretion (-52 (-121 to -71) v -31 (-44 to -18), and (-39 (-49 to 17) v (-22 (-39 to -3)), respectively). Sodium and chloride movement paralleled that of fluid. In conclusion, these data show that 5-HT and 5-HT3 receptors play an important part in cholera toxin induced secretion but are not involved in E coli heat stable or heat labile toxin induced secretion.

Animals↗
PubMed1990

Hepatobiliary compensation for the loss of gallbladder function after cholecystectomy. An experimental study in the cat.

The side effects of the removal of a functioning gallbladder are surprisingly few, and it has been suggested, but never demonstrated, that the hepatobiliary tract then adjusts to compensate for the loss of gallbladder function. In this study the effects of cholecystectomy on bile acid kinetics, bile flow, and biliary clearance of mannitol were studied in cats 6-8 weeks after cholecystectomy. An enhanced recycling rate of a diminished bile acid pool was found. The bile flow was reduced and the bile acid concentration in hepatic bile was increased, but fasting bile acid secretion rate was not changed. Both when the bile acid secretion rate was reduced by drainage via an acute bile fistula and when it was enhanced by intravenous infusion of glycocholic acid, there was a lower bile acid-independent flow in the cholecystectomy group. This reduced bile flow after cholecystectomy was not explained by the higher proportion of deoxycholic acid present in the bile of the cholecystectomized animals. Biliary clearance of mannitol, which is supposed to reflect the canalicular inflow, was not reduced, indicating that the reduction in bile flow is explained by a reduced fluid secretion or an enhanced fluid reabsorption in the bile ductules and ducts after cholecystectomy. In this manner the bile ducts compensate for the loss of the absorptive function of the gallbladder after cholecystectomy.

Animals↗
PubMed1992

Reduction of aspirin-induced gastric damage in rats by interleukin-1 beta: possible involvement of endogenous corticosteroids.

Administration of interleukin-1 (IL-1; 0.01-3 microgram/kg) by either i.p. or intragastric routes to rats reduced aspirin-induced gastric damage. These effects of IL-1 were not subject to desensitization by its pretreatment and were obtained without modification of the acute anti-inflammatory efficacy of aspirin. Gastroprotection could be effected without major modification of gastric tissue to form prostaglandins I2 or E2. A dose-related decrease of the acidic gastric fluid secretion induced by aspirin was observed with i.p. administered IL-1 was found to reduce gastric fluid volume only at the highest dose tested, although this was not associated with increased gastroprotection. By using adrenalectomized rats the gastric damage induced by aspirin was increased approximately 3-fold. IL-1 treatment, albeit with higher dosage, again reduced lesion formation. Treatment of adrenalectomized rats with dexamethasone and IL-1 synergistically reduced the gastric damage caused by aspirin. In normal rats these treatments caused only an additive reduction of lesion formation although the presence of endogenous glucocorticoid in these animals may mask any effects of the exogenously administered dexamethasone. The glucocorticoid-receptor antagonist, RU 38486, also potentiated aspirin-induced gastric damage and reduced the gastroprotective efficacy of IL-1 without modifying its effect on gastric fluid volume. The data indicate that gastroprotective actions of IL-1 are unlikely to be related upon effects on prostaglandin synthesis or gastric secretion. Endogenous glucocorticoids appear to have a modulatory role in controlling the severity of gastric damage evoked by aspirin and may potentiate the protective actions of IL-1.

Adrenalectomy↗
PubMed1995

[Study on the mechanisms of diarrhea induced by a new anticancer camptothecin derivative, irinotecan hydrochloride (CPT-11), in rats].

We investigated the mechanisms of CPT-11-induced diarrhea. 1) CPT-11 (80 mg/kg, i.v.) induced watery diarrhea within 1 hr after dosing in saline-loaded (10 ml/kg, p.o.) rats. This was partially inhibited by subcutaneous injection of atropine (1 mg/kg) or ondansetron (1 mg/kg) and almost completely inhibited by a combination of atropine and ondansetron or by clonidine (0.3 mg/kg) or morphine (10 mg/kg) alone. 2) CPT-11 at the same dose reduced intestinal fluid absorption, which was blocked by the anti-diarrheal agents mentioned above. Intraluminal injection of CPT-11 (20 mg/2 ml) inhibited fluid absorption and induced fluid secretion. 3) CPT-11, 60 mg/kg, by single intravenous injection induced fewer enzymological and histological changes in the small intestine than 5-FU at 270 mg/kg, while 4 consecutive dosings of CPT-11 induced delayed diarrhea (days 5-7) associated with disruption of intestinal integrity. Co-administration with anti-diarrheal agents, except for ondansetron, protected against watery diarrhea appearing within 1 hr after CPT-11 on days 3 and 4, but worsened delayed diarrhea. These results suggest that single injection of higher doses of CPT-11 causes watery diarrhea at an acute phase at least partly by reducing fluid absorption or increasing secretion, and that while conventional anti-diarrheal agents protect against watery diarrhea, their co-administration in repeated CPT-11 administration has no ameliorative effect on CPT-11-induced delayed diarrhea.

Animals↗
PubMed2006

Cholecystokinin- and gastrin-induced protein and amylase secretion from the parotid gland of the anaesthetized rat.

I.V. infusion of pentagastrin (20 microg/kg/h) or cholecystokinin (CCK)-8 (1 microg/kg/h) for 10 min caused secretion of salivary proteins from the parotid gland in the anaesthetized rat without any accompanying overt fluid secretion. This "occult" response was revealed by a subsequent wash-out injection of methacholine (5 microg/kg, I.V.) 10 min after the end of the infusion period (aiming at avoiding synergistic interactions). While the fluid response to methacholine was unaffected by the preceding infusion of pentagastrin and CCK-8, the output of protein increased by 147% (pentagastrin) and 74% (CCK-8) and that of amylase by 45% (CCK-8) compared to the responses to methacholine upon saline infusion. Those increases were abolished by the CCK-A receptor blocker (lorglumide), but not by the CCK-B receptor blocker (itriglumide). Evisceration, combined sympathetic and parasympathetic denervation of the glands and assay under adrenoceptor blockade excluded contribution from the gastro-intestinal tract, central or ganglionic mechanisms and circulating catecholamines to the increase in protein/amylase. Furthermore, Western blot demonstrated CCK receptors for both A and B subtypes in normal and chronically denervated glands. In the submandibular gland, both pentagastrin and CCK-8 evoked a trace secretion of saliva but, under the present experimental set-up, no statistically significant increase in protein output. Thus, in addition to the autonomic nervous system, gastrointestinal hormones may, in some types of glands, be involved in the secretion of salivary gland proteins.

Amylases↗
PubMed1976

Oestrogenic sensitivity of rat uterine secretion.

Ovariectomized adult rats with closed uteri were treated for 7 days with different oral and s..c. doses of oestradiol, oestrone, oestriol and ethinyl oestradiol. All treatments elicited the production of uterine fluid and the potencies of oestrogens were related to the amount of fluid secreted. Ethinyl oestradiol and oestradiol displayed similar activity when given s.c. A daily dose of 0-003 mg oestradiol/kg resulted in about 700 mg fluid. Oestrone was 3-10 times and oestriol about 100 times less active. Orally, ethinyl oestradiol was the most potent substance and 700 mg secretion was obtained with a dose of 0-03 mg/kg daily. Oestradiol was about 30 times, oestrone about 100 times and oestriol 50 times less active than ethinyl oestradiol by this route. The viscosity of the secretion was unaffected, remaining between 1-6 and 2-4 cP. The pH of the fluid did not change, but that of the uterine lumen diminished slightly. These effects of oestrogens were associated with an increase in the weight of the empty uterus and a decrease in body weight.

Animals↗
PubMed1993

Necturus gallbladder epithelial cell volume regulation and inhibitors of arachidonic acid metabolism.

Inhibition of the metabolism of arachidonic acid by the epoxygenase (cytochrome P-450) pathway with the inhibitor ketoconazole results in excessive cell swelling upon exposure to hyposmolality instead of the rapid and complete regulatory volume decrease (RVD) normally observed. NaCl entry from bathing solutions to cell interior was shown to cause this swelling, with Na influx occurring across the basolateral membrane and electrically silent Cl influx across the apical membrane. Ion substitution experiments show that the KCl efflux mediating RVD was unimpaired by ketoconazole, but was overwhelmed by the NaCl influx. Measurements of transepithelial fluid flux, Cl concentration, osmolality and pH showed that gallbladders treated with ketoconazole transiently secreted fluid rather than the normal absorption. We conclude that inhibition of arachidonic acid metabolism does not directly affect RVD by Necturus gallbladder, but that blockade of the epoxygenase pathway can have a profound influence on NaCl entry into gallbladder epithelial cells.

Animals↗