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At least 811 records · Page 45Linked to original sources
PubMed2002

A novel chloride conductance activated by extracellular ATP in mouse parotid acinar cells.

Salivary gland fluid secretion is driven by transepithelial Cl- movement involving an apical Cl- channel whose molecular identity remains unknown. Extracellular ATP (ATP(o)) has been shown to activate a Cl- conductance (I(ATPCl)) in secretory epithelia; to gain further insight into I(ATPCl) in mouse parotid acinar cells, we investigated the effects of ATP(o) using the whole-cell patch-clamp technique. ATP(o) and 2'- and 3'-O-(4-benzoylbenzoyl)adenosine 5'-triphosphate triethylammonium salt (Bz-ATP) produced concentration-dependent, time-independent Cl- currents with an EC50 of 160 and 15 microM, respectively. I(ATPCl) displayed a selectivity sequence of SCN- > I- = NO3- > Cl- > glutamate, similar to the Cl- channels activated by Ca2+, cAMP and cell swelling in acinar cells. In contrast, I(ATPCl) was insensitive to pharmacological agents that are known to inhibit these latter Cl- channels, was independent of Ca2+ and was not regulated by cell volume. Moreover, the I(ATPCl) magnitude from wild-type animals was comparable to that from mice with null mutations in the Cftr, Clcn3 and Clcn2 Cl- channel genes. Taken together, our results demonstrate that I(ATPCl) is distinct from the channels described previously in acinar cells. The activation of I(ATPCl) by Bz-ATP suggests that P2 nucleotide receptors are involved. However, inhibition of G-protein activation with GDP-beta-S failed to block I(ATPCl), and Cibacron Blue 3GA and 4,4'-diisothyocyanostilbene-2,2'-disulphonic disodium salt selectively inhibited the Na+ currents (presumably through P2X receptors) without altering I(ATPCl), suggesting that neither P2Y nor P2X receptors are likely to be involved in I(ATPCl) activation. We conclude that I(ATPCl) is not associated with Cl- channels previously characterized in mouse parotid acinar cells, nor is it dependent on P2 nucleotide receptor stimulation. I(ATPCl) expressed in acinar cells reflects the activation of a novel ATP-gated Cl- channel that may play an important physiological role in salivary gland fluid secretion.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2000

Blockade of isoprenaline-induced fluid and protein secretion by the mandibular glands of the red kangaroo, Macropus rufus, with selective antagonists.

Selective and non-selective beta-adrenoceptor antagonists were used to block the increases in fluid and protein secretion caused by sympathomimetic stimulation of the mandibular gland of red kangaroos during intracarotid infusion of isoprenaline. Atenolol or ICI118551 at antagonist:agonist ratios up to 300:1 caused increasing but incomplete blockade of fluid secretion and protein release. Both selective antagonists had equal potency and both antagonists were more effective at blocking protein release than at blocking fluid secretion. Consequently, the mechanisms underpinning fluid secretion are more sensitive to beta-sympathomimetic stimulation than those causing protein release. Propranolol at antagonist:agonist ratios of 300:1 was more potent than the selective antagonists, almost totally blocking the increases in fluid secretion and protein release. The data are consistent with the acini of the kangaroo mandibular gland having both beta(1)- and beta(2)-adrenoceptors and with the increased fluid secretion and protein release by isoprenaline being mediated by both receptor subtypes.

Adrenergic beta-1 Receptor Antagonists↗
PubMed1989

Effects of muscarinic, alpha-adrenergic, and substance P agonists and ionomycin on ion transport mechanisms in the rat parotid acinar cell. The dependence of ion transport on intracellular calcium.

The relationship between receptor-mediated increases in the intracellular free calcium concentration [( Ca]i) and the stimulation of ion fluxes involved in fluid secretion was examined in the rat parotid acinar cell. Agonist-induced increases in [Ca]i caused the rapid net loss of up to 50-60% of the total content of intracellular chloride (Cli) and potassium (Ki), which is consistent with the activation of calcium-sensitive chloride and potassium channels. These ion movements were accompanied by a 25% reduction in the intracellular volume. The relative magnitudes of the losses of Ki and the net potassium fluxes promoted by carbachol (a muscarinic agonist), phenylephrine (an alpha-adrenergic agonist), and substance P were very similar to their characteristic effects on elevating [Ca]i. Carbachol stimulated the loss of Ki through multiple efflux pathways, including the large-conductance Ca-activated K channel. Carbachol and substance P increased the levels of intracellular sodium (Nai) to more than 2.5 times the normal level by stimulating the net uptake of sodium through multiple pathways; Na-K-2Cl cotransport accounted for greater than 50% of the influx, and approximately 20% was via Na-H exchange, which led to a net alkalinization of the cells. Ionomycin stimulated similar fluxes through these two pathways, but also promoted sodium influx through an additional pathway which was nearly equivalent in magnitude to the combined uptake through the other two pathways. The carbachol-induced increase in Nai and decrease in Ki stimulated the activity of the sodium pump, measured by the ouabain-sensitive rate of oxygen consumption, to nearly maximal levels. In the absence of extracellular calcium or in cells loaded with the calcium chelator BAPTA (bis[o-aminophenoxy]ethane-N,N,N',N'-tetraacetic acid) the magnitudes of agonist- or ionomycin-stimulated ion fluxes were greatly reduced. The parotid cells displayed a marked desensitization to substance P; within 10 min the elevation of [Ca]i and alterations in Ki, Nai, and cell volume spontaneously returned to near baseline levels. In addition to quantitating the activation of various ion flux pathways in the rat parotid acinar cell, these results demonstrate that the activation of ion transport systems responsible for fluid secretion in this tissue is closely linked to the elevation of [Ca]i.

Adrenergic alpha-Agonists↗
PubMed2000

The inhibition of cholera toxin-induced 5-HT release by the 5-HT(3) receptor antagonist, granisetron, in the rat.

1. The secretagogue 5-hydroxytryptamine (5-HT) is implicated in the pathophysiology of cholera. 5-HT released from enterochromaffin cells after cholera toxin exposure is thought to activate non-neuronally (5-HT(2) dependent) and neuronally (5-HT(3) dependent) mediated water and electrolyte secretion. CT-secretion can be reduced by preventing the release of 5-HT. Enterochromaffin cells possess numerous receptors that, under basal conditions, modulate 5-HT release. 2. These include basolateral 5-HT(3) receptors, the activation of which is known to enhance 5-HT release. 3. Until now, 5-HT(3) receptor antagonists (e.g. granisetron) have been thought to inhibit cholera toxin-induced fluid secretion by blockading 5-HT(3) receptors on secretory enteric neurones. Instead we postulated that they act by inhibiting cholera toxin-induced enterochromaffin cell degranulation. 4. Isolated intestinal segments in anaesthetized male Wistar rats, pre-treated with granisetron 75 microg kg(-1), lidoocaine 6 mg kg(-1) or saline, were instilled with a supramaximal dose of cholera toxin or saline. Net fluid movement was determined by small intestinal perfusion or gravimetry and small intestinal and luminal fluid 5-HT levels were determined by HPLC with fluorimetric detection. 5. Intraluminal 5-HT release was proportional to the reduction in tissue 5-HT levels and to the onset of water and electrolyte secretion, suggesting that luminal 5-HT levels reflect enterochromaffin cell activity. 6. Both lidocaine and granisetron inhibited fluid secretion. However, granisetron alone, and proportionately, reduced 5-HT release. 7. The simultaneous inhibition of 5-HT release and fluid secretion by granisetron suggests that 5-HT release from enterochromaffin cells is potentiated by endogenous 5-HT(3) receptors. The accentuated 5-HT release promotes cholera toxin-induced fluid secretion.

Animals↗
PubMed1994

Cystic fibrosis heterozygote resistance to cholera toxin in the cystic fibrosis mouse model.

The effect of the number of cystic fibrosis (CF) alleles on cholera toxin (CT)-induced intestinal secretion was examined in the CF mouse model. CF mice that expressed no CF transmembrane conductance regulator (CFTR) protein did not secrete fluid in response to CT. Heterozygotes expressed 50 percent of the normal amount of CFTR protein in the intestinal epithelium and secreted 50 percent of the normal fluid and chloride ion in intestinal epithelium and secreted 50 percent of the normal fluid and chloride ion and fluid secretion suggests that CF heterozygotes might possess a selective advantage of resistance to cholera.

Alleles↗
PubMed1991

Ontogeny of ion transport across fetal pulmonary epithelial cells in monolayer culture.

The transition of the fetal lung from a fluid-secreting to a fluid-absorbing organ is dependent on ion transport across the pulmonary epithelium. This study examined the ion transport characteristics of distal pulmonary epithelial cells isolated from rat fetuses in late gestation and maintained in differentiation-arrested monolayer cultures. The response to inhibitors of active ion transport suggested the presence of apical to basolateral Na+ transport in monolayers derived from each gestational age. However, amiloride inhibition of short-circuit current (Isc) varied with gestational age, decreasing Isc by 30% in monolayers derived from day 18 fetuses and by 55% in monolayers from day 21 fetuses. A portion (10%) of the residual Isc remaining after amiloride addition to monolayers from day 18 fetuses could be inhibited by bumetanide, suggesting the induction of net Cl- transport. Ion-substitution experiments confirmed the presence of Na+ and inducible Cl- transport mechanisms in monolayers from day 18 fetuses and only Na+ transport mechanisms in monolayers from day 21 fetuses. beta-Adrenergic stimulation increased Isc but maintained the age-dependent characteristics of Na(+)- and Cl(-)-dependent ion transport. In summary, monolayer cultures of fetal pulmonary epithelial cells exhibit age-dependent differences in ion transport properties that are consistent with a transition or maturation of the distal pulmonary epithelium from an epithelium capable of Na+ absorption and Cl- secretion preterm to one capable of only Na+ absorption at term.

Amiloride↗
PubMed1996

Increased Po2 alters the bioelectric properties of fetal distal lung epithelium.

At birth the lung must efficiently clear the liquid from its air spaces and permanently convert from a fluid-secreting to a fluid-absorbing organ. When primary cultures of rat fetal distal lung epithelium (FDLE) grown on permeable supports were switched from a fetal (3%) to a postnatal (21%) oxygen environment, there was an increase in epithelial permeability as reflected by a dose-dependent decline in transepithelial resistance (Rt) 4 h later (3% = 239 +/- 19 omega.cm2; 21% = 170 +/- 28 omega.cm2; 50% = 98 +/- 20 omega.cm2; P < 0.05). The effect was transient, since monolayers initially maintained at 3% and switched to these higher oxygen concentrations subsequently had Rt values comparable to the 3% group at 48 h (3% = 153 +/- 17 omega.cm2; 21% = 181 +/- 19 omega.cm2; 50% = 192 +/- 21 omega.cm2; P = NS). Changes in Rt were associated with expected changes in the histological appearance of the interepithelial tight junctions, but intracellular actin content and distribution remained constant. Amiloride-sensitive equivalent short-circuit current increased within 18 h, with further increases after 48 h of exposure to postnatal oxygen concentrations. Ion substitution experiments suggested diminished FDLE Cl transport and increased Na transport. The amount of FDLE-alpha, -beta, and -gamma rat epithelial Na channel mRNA increased within 48 h of increasing the ambient oxygen concentration. These results suggest that the physiological increase in alveolar Po2 at birth is, at least in part, responsible for distal lung's permanent switch from Cl secretion to Na absorption at birth.

Animals↗
PubMed1995

Inhibition of Ca(2+)-dependent Cl- channels from secretory epithelial cells by low internal pH.

The actions of intracellular pH (pHi) on Ca(2+)-dependent Cl- channels were studied in secretory epithelial cells derived from human colon carcinoma (T84) and in isolated rat parotid acinar cells. Channel currents were measured with the whole cell voltage clamp technique with pipette solutions of different pH. Ca(2+)-dependent Cl- channels were activated by superfusing ionomycin to increase the intracellular calcium concentration ([Ca2+]i) or by using pipette solutions with buffered Ca2+ levels. Large currents were activated in T84 and parotid cells by both methods with pHi levels of 7.3 or 8.3. Little or no Cl- channel current was activated with pHi at 6.4. We used on-cell patch clamp methods to investigate the actions of low pHi on single Cl- channel current amplitude in T84 cells. Lowering the pHi had little or no effect on the current amplitude of a 8 pS Cl- channel, but did reduce channel activity. These results suggest that cytosolic acidification may be able to modulate stimulus-secretion coupling in fluid-secreting epithelia by inhibiting the activation of Ca(2+)-activated Cl- channels.

Animals↗
PubMed1983

Quantitation and origin of immunoglobulins A, G and M in the secretions and fluids of the reproductive tract of the sow.

Immunoglobulin quantitation of fluids obtained from several regions of the female reproductive tract indicated the presence of IgG, IgA and IgM. IgG was almost invariably present in greatest amounts and IgM always made the smallest contribution. Although much of this immunoglobulin was derived from serum, evidence of the molecular size of IgA, the IgA and IgG ratios and that obtained from experiments involving the injection into sows of 125I-labelled immunoglobulin indicated that local synthesis within the tract also occurred.

Animals↗
PubMed1984

Colonic absorption and secretion of fluids, electrolytes and organic acids in East African wild ruminants.

In sixteen species of wild ruminants colonic absorption of fluids averaged 48% of the fluids entering the large bowel. Values ranged from 26% (steenbok) to 65% (gerenuk). Absorption of sodium, potassium, chloride and organic acids were variable between species. Colonic absorption of potassium ions were found to be related to diet selection and body weight of the animals. colonic absorption of volatile fatty acids were significantly greater in browsers (28.4 mmol/l) than grazers (9.6 mmol/l). The African buffalo are the only species of wild ruminants not forming a faecal pellet; colonic functions were not different from those species forming faecal pellets.

Absorption↗
PubMed2004

Functions and roles of the extracellular Ca2+-sensing receptor in the gastrointestinal tract.

The gastrointestinal tract is vital to food digestion and nutrient absorption as well as normal salt and water homeostasis. Studies over the last several years have shown that the Ca2+-sensing receptor is expressed along the entire gastrointestinal tract. The potential roles for the receptor in gastrointestinal biology are now only beginning to be elucidated and much work remains. Well-studied physiological effects include regulation of gastric acid secretion and modulation of fluid transport in the colon. It remains to be determined if the Ca2+-sensing receptor is involved in calcium handling by the gastrointestinal tract. The ability of organic nutrient receptor agonists/allosteric modifiers, such as polyamines and L-amino acids, to activate the Ca2+-sensing receptor suggest potential roles in signalling nutrient availability to gastric and intestinal epithelial cells. In addition, polyamines are crucial for normal cell proliferation and differentiation required to sustain the rapid turnover of gastrointestinal epithelial cells and the Ca2+-sensing receptor may be involved in this function. Activation of the colonic Ca2+-sensing receptor can abrogate cyclic nucleotide-mediated fluid secretion suggesting a role for the receptor in modifying secretory diarrheas like cholera. Finally, the Ca2+-sensing receptor has been suggested to provide a mechanism for the effect of calcium intake in reducing the risk of colon cancer.

Animals↗
PubMed2002

Where have all the Na+ channels gone? In search of functional ENaC in exocrine pancreas.

Many epithelia express specific Na(+) channels (ENaC) together with the cystic fibrosis regulator (CFTR) Cl(-) channels. Pancreatic ducts secrete HCO(3)(-)-rich fluid and express CFTR. However, the question whether they possess ENaC has not been consistently addressed. The aim of the present study was to investigate if pancreatic ducts express functional ENaC. Membrane voltages (V) of ducts isolated from rat pancreas were measured with microelectrodes or whole-cell patch-clamp technique. Amiloride and benzamil given from bath or luminal sides did not hyperpolarize V. Lowering of extracellular Na(+) concentrations had effects that were not consistent with a simple Na(+) conductance, but rather with a Na(+)/Ca(2+) exchange. Acute or long-lasting treatment of pancreatic ducts with mineralocorticoids had no effect on V of unstimulated or secretin-stimulated preparations. Furthermore, pre-treatment of animals with glucocorticoids had no effect on pancreatic fluid secretion evoked from ducts, or from acini. Hence, our study shows that pancreas especially pancreatic ducts do not express functional ENaC.

Amiloride↗
PubMed1999

Dynamics of prostaglandin secretion, intrauterine fluid and uterine clearance in reproductively normal mares and mares with delayed uterine clearance.

Two experiments were performed to investigate relationships between oxytocin, prostaglandin release, uterine emptying and fluid accumulation in the uterus. In Experiment 1, the effect of oxytocin on the pattern of prostaglandin release during uterine clearance of radiocolloid was measured in 5 normal mares and 5 mares with delayed uterine clearance. Uterine clearance was measured during estrus by scintigraphy at 0, 60 and 120 min after colloid infusion. After the 120-min reading, 20 IU, i.v., oxytocin were given, and the amount of colloid cleared was measured at 135, 150 and 180 min. Plasma was obtained prior to and during scintigraphy at 5- and 15-min intervals to measure concentrations of 15-keto-13,14-dihydro-PGF2 alpha metabolite (PGFM) by RIA. In Experiment 2, plasma PGFM levels were compared after administration of oxytocin in 8 normal mares and 6 mares with delayed uterine clearance to determine if intrauterine fluid stimulated prostaglandin release. Mares received 2 treatments in a cross-over design. Treatment 1 consisted of 20 IU, i.v., oxytocin during estrus. Treatment 2 consisted of an infusion of 10 mL, i.u., saline 15 min prior to oxytocin administration. Treatments were performed 4 to 6 h apart. Blood was collected and PGFM was measured as in experiment 1. Data were analyzed by least squares analysis of variance. In Experiment 1, regression analysis of scintigraphy and PGFM profiles indicated that time response curves differed between groups (P < 0.01). At 120 min, normal mares retained 40.4 +/- 4.9% (mean +/- SEM) of the radiocolloid while mares with delayed clearance retained 88 +/- 5%. Fifteen minutes after oxytocin administration (135 min), all normal mares and 4 of 5 mares with delayed clearance retained only < 6% of the colloid. During the first 120 min, plasma PGFM concentrations did not differ between the 2 groups. After oxytocin was given, plasma PGFM concentrations increased in 4 of 5 mares with delayed uterine clearance (80 to 3,096 pg/mL) but not in normal mares (13 to 46 pg/mL). In Experiment 2, plasma PGFM concentrations did not rise in normal mares but rose in 3 of 6 mares with delayed clearance (135 to 483 pg/mL) independent of treatment or period. The results suggest that intrauterine clearance of radiocolloid after oxytocin administration appears to be independent of PGF2 alpha release in normal mares during estrus. The difference in prostaglandin release response after oxytocin administration between the 2 groups was unrelated to the presence of intrauterine fluid.

Animals↗