Chloride secretion and conductance of teleost opercular membrane: effects of prolactin

1982 ◽  
Vol 242 (3) ◽  
pp. R380-R389 ◽  
Author(s):  
J. K. Foskett ◽  
T. E. Machen ◽  
H. A. Bern
Keyword(s):  
Active Transport ◽  
Short Circuit ◽  
Chloride Secretion ◽  
Alternative Interpretation ◽  
Chloride Cells ◽  
Dependent Manner ◽  
Transport Pathway ◽  
Accurate Analysis ◽  
Equivalent Circuit Analysis ◽  
Fish Yield

Effects of prolactin on transport properties of opercular membranes from seawater-adapted tilapia, Sarotherodon mossambicus, have been examined. These membranes are high conductance (average Gt approximately 4 mS.cm-2) tissues with short-circuit currents (I) equal to net chloride secretion. Despite high Gt, nonlinear current-voltage relationships suggest that opercular membranes cannot be classified as "leaky" tissues. Variability among membranes is reflected in a linear relationship between I and Gt with a slope equal to 26 mV and the zero-current Gt intercept equal to 0.45 mS.cm-2. Prolactin injections decrease I and Gt in a dose-dependent manner. Phosphodiesterase inhibition, without effect on I in untreated fish, often partially reverses these prolactin effects. Gt-I data from prolactin-treated fish yield a slope of 18 mV and a Gt intercept of 0.10 mS.cm-2. The effects of prolactin are discussed in terms of conventional equivalent circuit analysis. Discrepancies between predictions based on this model and the actual data indicate that an alternative interpretation, based on a heterogeneous cell population, is more accurate. Analysis of this circuit suggests that the ratio of paracellular to active transport pathway conductances associated with chloride cells is constant and that differences in Gt and I are due to parallel changes in these conductances. Prolactin may effectively "remove" chloride cells from these membranes as well as inhibit (reversible by elevated cellular cAMP levels) active transport pathway conductance of remaining cells.

scholarly journals Chloride cells and the hormonal control of teleost fish osmoregulation

1983 ◽  
Vol 106 (1) ◽  
pp. 255-281 ◽  
Author(s):  
J. K. Foskett ◽  
H. A. Bern ◽  
T. E. Machen ◽  
M. Conner
Keyword(s):  
Active Transport ◽  
Teleost Fish ◽  
Sea Water ◽  
Short Circuit ◽  
Chloride Secretion ◽  
Hormonal Control ◽  
Chloride Cell ◽  
Chloride Cells ◽  
Accessory Cell ◽  
Nacl Transport

Teleost fish osmoregulation is largely the result of integrated transport activities of the gill, gut and renal system. The basic ‘epithelial fabric’ in each of these tissues is adapted to provide the appropriate transport mechanisms depending upon whether the fish is in fresh water or sea water. Net NaCl transport by the branchial epithelium reverses direction when euryhaline species migrate between the two media, providing a useful focus in experiments designed to elucidate mechanisms of differentiation and integration of transport function. Isolated opercular membranes and skins from certain seawater-adapted species are good models to study branchial salt extrusion mechanisms. These heterogeneous tissues generate short-circuit currents equal to net chloride secretion. The vibrating probe technique has allowed localization of all current and almost all conductance to the apical crypt of chloride cells. Area-specific surface current and conductance of chloride cells are 18 mA cm-2 and 580 mS cm-2 (1.7 omega cm2), ranking them as one of the most actively transporting and conductive cells known. There is no net sodium transport under short-circuit conditions but the chloride secretion process is sodium-dependent and ouabain and ‘loop’-diuretic sensitive. Sodium fluxes through chloride cells are large (PNa = 5.2 X 10(−4) cms-1) nd appear passive and rate-limited by a single barrier. A link may exist between the active transport and leak pathways since sodium fluxes always account for 50% of chloride cell conductance. The sodium pathway is probably the chloride cell-accessory cell tight junction, although this is still unresolved. Chloride secretion can be rapidly modulated by several hormones, including catecholamines, somatostatin, glucagon, vasoactive intestinal polypeptide and urotensins I and II. Regulation by these hormones may be by rapid alterations of cellular cAMP levels. Differentiation of chloride cells and chloride secretion may be controlled by cortisol and prolactin. Cortisol stimulates chloride cell proliferation and differentiation and appears to interact with NaCl to initiate salt secretion. Prolactin appears to cause chloride cell dedifferentiation by reducing both the active-transport and leak pathways proportionately.(ABSTRACT TRUNCATED AT 400 WORDS)

Functional characterization and expression of PBR in rat gastric mucosa: stimulation of chloride secretion by PBR ligands

2004 ◽  
Vol 286 (6) ◽  
pp. G1069-G1080 ◽  
Author(s):  
M. A. Ostuni ◽  
K. Marazova ◽  
G. Peranzi ◽  
B. Vidic ◽  
V. Papadopoulos ◽  
...  
Keyword(s):  
Gastric Mucosa ◽  
Short Circuit ◽  
Functional Characterization ◽  
Benzodiazepine Receptor ◽  
Chloride Secretion ◽  
Parietal Cells ◽  
Receptor Protein ◽  
Antral Mucosa ◽  
Dependent Manner ◽  
Calcium Depletion

Previous studies have demonstrated that gastric mucosa contained high levels of the polypeptide diazepam binding inhibitor, the endogenous ligand of the peripheral-type benzodiazepine receptor (PBR). However, the expression and function of this receptor protein in these tissues have not been investigated. Immunohistochemistry identified an intense PBR immunoreactivity in the mucous and parietal cells of rat gastric fundus and in the mucous cells of antrum. Immunoelectron microscopy revealed the mitochondrial localization of PBR in these cells. Binding of isoquinoline PK 11195 and benzodiazepine Ro5–4864 to gastric membranes showed that fundus had more PBR-binding sites than antrum, displaying higher affinity for PK 11195 than Ro5–4864. In a Ussing chamber, PK 11195 and Ro5–4864 increased short-circuit current ( Isc) in fundic and antral mucosa in a concentration-dependent manner in the presence of GABAA and central benzodiazepine receptor (CBR) blockers. This increase in Isc was abolished after external Cl− substitution and was sensitive to chloride channels or transporter inhibitors. PK 11195-induced chloride secretion was also 1) sensitive to verapamil and extracellular calcium depletion, 2) blocked by thapsigargin and intracellular calcium depletion, and 3) abolished by the mitochondrial pore transition complex inhibitor cyclosporine A. PK 11195 had no direct effect on H+ secretion, indicating that it stimulates a component of Cl− secretion independent of acid secretion in fundic mucosa. These data demonstrate that mucous and parietal cells of the gastric mucosa express mitochondrial PBR functionally coupled to Ca2+-dependent Cl− secretion, possibly involved in the gastric mucosa protection.

scholarly journals Glucagon-like peptide-1 modulates neurally evoked mucosal chloride secretion in guinea pig small intestine in vitro

2012 ◽  
Vol 302 (3) ◽  
pp. G352-G358 ◽  
Author(s):  
Sara Baldassano ◽  
Guo-Du Wang ◽  
Flavia Mulè ◽  
Jackie D. Wood
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Receptor Antagonist ◽  
Vasoactive Intestinal Peptide ◽  
Short Circuit ◽  
Chloride Secretion ◽  
Dependent Manner ◽  
Evoked Responses ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Glucagon-like peptide-1 (GLP-1) acts at the G protein-coupled receptor, GLP-1R, to stimulate secretion of insulin and to inhibit secretion of glucagon and gastric acid. Involvement in mucosal secretory physiology has received negligible attention. We aimed to study involvement of GLP-1 in mucosal chloride secretion in the small intestine. Ussing chamber methods, in concert with transmural electrical field stimulation (EFS), were used to study actions on neurogenic chloride secretion. ELISA was used to study GLP-1R effects on neural release of acetylcholine (ACh). Intramural localization of GLP-1R was assessed with immunohistochemistry. Application of GLP-1 to serosal or mucosal sides of flat-sheet preparations in Ussing chambers did not change baseline short-circuit current ( Isc), which served as a marker for chloride secretion. Transmural EFS evoked neurally mediated biphasic increases in Iscthat had an initial spike-like rising phase followed by a sustained plateau-like phase. Blockade of the EFS-evoked responses by tetrodotoxin indicated that the responses were neurally mediated. Application of GLP-1 reduced the EFS-evoked biphasic responses in a concentration-dependent manner. The GLP-1 receptor antagonist exendin-(9–39) suppressed this action of GLP-1. The GLP-1 inhibitory action on EFS-evoked responses persisted in the presence of nicotinic or vasoactive intestinal peptide receptor antagonists but not in the presence of a muscarinic receptor antagonist. GLP-1 significantly reduced EFS-evoked ACh release. In the submucosal plexus, GLP-1R immunoreactivity (IR) was expressed by choline acetyltransferase-IR neurons, neuropeptide Y-IR neurons, somatostatin-IR neurons, and vasoactive intestinal peptide-IR neurons. Our results suggest that GLP-1R is expressed in guinea pig submucosal neurons and that its activation leads to a decrease in neurally evoked chloride secretion by suppressing release of ACh at neuroepithelial junctions in the enteric neural networks that control secretomotor functions.

Effect of atriopeptin II on isolated opercular epithelium of Fundulus heteroclitus

1988 ◽  
Vol 254 (1) ◽  
pp. R27-R32 ◽  
Author(s):  
J. I. Scheide ◽  
J. A. Zadunaisky
Keyword(s):  
Fundulus Heteroclitus ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Chloride Cells ◽  
Induced Response ◽  
Ion Regulation ◽  
Cyclic Monophosphate ◽  
Stimulation Of

The effect of atriopeptin II (ANF) on the in vitro opercular epithelium was investigated by use of short-circuit current techniques. Serosal addition of ANF stimulates chloride secretion (short-circuit current) 19% above control values with a 7% increase in tissue conductance. Mucosal addition of ANF to the opercular epithelium was without effect. The ANF stimulation of the current was dose dependent with a maximum at 10(-7) M. The addition of ANF had no effect on the current or the conductance of opercular epithelia bathed in Cl--free Ringer. The opercular current could be stimulated above the ANF response by isoproterenol (10(-6) M). Pretreatment of the opercular epithelium with propranolol (10(-5) M) did not inhibit the stimulation of the short-circuit current by ANF but did inhibit the isoproterenol response indicating that the ANF stimulatory activity was independent of the beta-adrenergic receptors. The ANF-stimulated short-circuit current was found in operculi pretreated with tetrodotoxin (10(-6) or 10(-5) M) or diltiazem (10(-4) M) indicating the ANF response was not due to nerve stimulation. Pretreatment of opercular tissue with dibutyryl adenosine 3',5'-cyclic monophosphate, 8-bromoadenosine 3',5'-cyclic monophosphate, or 8-bromoguanosine 3',5'-cyclic monophosphate (10(-4) M) had no effect on the ANF stimulatory response. Opercular epithelia from short-term freshwater-adapted killifish also showed the ANF-induced response. The stimulation of chloride secretion in Fundulus heteroclitus chloride cells by ANF may have a role in teleost ion regulation.

Hydrogen peroxide stimulates chloride secretion in primary inner medullary collecting duct cells via mPGES-1-derived PGE2

2007 ◽  
Vol 293 (5) ◽  
pp. F1571-F1576 ◽  
Author(s):  
Sunhapas Soodvilai ◽  
Zhanjun Jia ◽  
Tianxin Yang
Keyword(s):  
Collecting Duct ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Dependent Manner ◽  
Semipermeable Membranes ◽  
Nacl Transport ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct

We investigated the role and mechanism of H2O2 in regulation of NaCl transport in primary inner medullary collecting duct (IMCD) cells. IMCD cells were isolated from wild-type mice and grown onto semipermeable membranes, and short-circuit current ( Isc) was determined by Ussing chamber. Exposure of IMCD cells to H2O2 at a range of 100–300 μM caused a rapid increase in Isc in a time- and dose-dependent manner. This increase was almost abolished by the cystic fibrosis transmembrane conductance regulator (CFTR) Cl− channel inhibitors diphenylamine-2-carboxylic acid (DPC) and CFTRinhibitor-172. In contrast, the magnitude of stimulation was unaffected by the epithelial Na+ channel (ENaC) inhibitor amiloride. The H2O2-induced Cl− secretion was significantly inhibited by indomethacin, as well as by microsomal PGE synthase-1 (mPGES-1) deficiency. Like H2O2, PGE2 treatment induced a twofold increase in Isc that was reduced by the protein kinase A (PKA) inhibitors H-89 and KT5720. These data suggest that H2O2 stimulates CFTR Cl− channel-mediated Cl− secretion through cyclooxygenase- and mPGES-1-dependent release of PGE2 and subsequent activation of PKA.

scholarly journals Glucagon-like peptide-2 modulates neurally evoked mucosal chloride secretion in guinea pig small intestine in vitro

2009 ◽  
Vol 297 (4) ◽  
pp. G800-G805 ◽  
Author(s):  
Sara Baldassano ◽  
Sumei Liu ◽  
Mei-Hu Qu ◽  
Flavia Mulè ◽  
Jackie D. Wood
Keyword(s):  
Guinea Pig ◽  
Vasoactive Intestinal Peptide ◽  
Acetylcholine Release ◽  
Short Circuit ◽  
Chloride Secretion ◽  
Dependent Manner ◽  
Evoked Responses ◽  
Guinea Pig Ileum ◽  
Ussing Chambers ◽  
Glucagon Like Peptide

Glucagon-like peptide-2 (GLP-2) is an important neuroendocrine peptide in intestinal physiology. It influences digestion, absorption, epithelial growth, motility, and blood flow. We studied involvement of GLP-2 in intestinal mucosal secretory behavior. Submucosal-mucosal preparations from guinea pig ileum were mounted in Ussing chambers for measurement of short-circuit current ( Isc) as a surrogate for chloride secretion. GLP-2 action on neuronal release of acetylcholine was determined with ELISA. Enteric neuronal expression of the GLP-2 receptor (GLP-2R) was studied with immunohistochemical methods. Application of GLP-2 (0.1–100 nM) to the serosal or mucosal side of the preparations evoked no change in baseline Isc and did not alter transepithelial ionic conductance. Transmural electrical field stimulation (EFS) evoked characteristic biphasic increases in Isc, with an initially rapid rising phase followed by a sustained phase. Application of GLP-2 reduced the EFS-evoked biphasic responses in a concentration-dependent manner. The GLP-2R antagonist GLP-2-(3-33) significantly reversed suppression of the EFS-evoked responses by GLP-2. Tetrodotoxin, scopolamine, and hexamethonium, but not vasoactive intestinal peptide type 1 receptor (VPAC1) antagonist abolished or reduced to near zero the EFS-evoked responses. GLP-2 suppressed EFS-evoked acetylcholine release as measured by ELISA. Pretreatment with GLP-2-(3-33) offset this action of GLP-2. In the submucosal plexus, GLP-2R immunoreactivity (-IR) was expressed in choline acetyltransferase-IR neurons, somatostatin-IR neurons, neuropeptide Y-IR neurons, and vasoactive intestinal peptide-IR neurons. We conclude that submucosal neurons in the guinea pig ileum express GLP-2R. Activation of GLP-2R decreases neuronally evoked epithelial chloride secretion by suppressing acetylcholine release from secretomotor neurons.

Tyrosine phosphorylation is a novel pathway for regulation of chloride secretion in shark rectal gland

1995 ◽  
Vol 269 (4) ◽  
pp. F594-F600 ◽  
Author(s):  
R. W. Lehrich ◽  
J. N. Forrest
Keyword(s):  
Tyrosine Phosphorylation ◽  
Kinase Inhibitor ◽  
Chloride Transport ◽  
Short Circuit ◽  
Chloride Secretion ◽  
Rectal Gland ◽  
Dependent Manner ◽  
Camp Content ◽  
Tubular Cells ◽  
Genistein Treatment

We used the specific tyrosine kinase inhibitor genistein to define the involvement of tyrosine phosphorylation in the regulation of chloride transport in the rectal gland of the dogfish shark, a model for chloride secretion via a cystic fibrosis transmembrane conductance regulator (CFTR)-like channel. In the perfused gland, genistein (100 microM) promptly increased chloride secretion from basal values of 159 +/- 36 to 966 +/- 49 mueq.h-1.g-1 (P < 0.0001). Bumentanide fully reversed genistein-induced secretion. In primary culture monolayers of rectal gland tubular cells, genistein, but not the inactive 7-glucoside form, genistin, increased short-circuit current in a dose-dependent manner, from basal values of 2.7 +/- 4.3 to 104 +/- 10 microA/cm2 (P < 0.0001). Apically applied genistein induced significantly greater chloride secretion than basolateral addition. Genistein did not increase the adenosine 3',5'-cyclic monophosphate (cAMP) content of either perfused glands or cultured monolayers. Using an anti-phosphotyrosine antibody, we observed phosphorylation of multiple proteins. Four peptides, with molecular masses of 250, 210, 55, and 53 kDa, responded to genistein treatment with a decrease in tyrosine phosphorylation. These data demonstrate the following: 1) genistein induces bumetanide-sensitive chloride secretion in both perfused rectal glands and cultured tubular cells; 2) these effects are not accompanied by an elevation of tissue cAMP, indicating that genistein-induced secretion is not mediated by the cAMP-protein kinase A pathway; and 3) genistein-sensitive peptides are present in the rectal gland cell and are candidates for involvement in the regulation of chloride secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Action of pituitary adenylate cyclase-activating polypeptide on ion transport in guinea pig distal colon

1993 ◽  
Vol 264 (3) ◽  
pp. G433-G441 ◽  
Author(s):  
A. Kuwahara ◽  
Y. Kuwahara ◽  
T. Mochizuki ◽  
N. Yanaihara
Keyword(s):  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Ion Transport ◽  
Short Circuit ◽  
Distal Colon ◽  
Chloride Secretion ◽  
Dependent Manner ◽  
Evoked Responses ◽  
Concentration Dependent Manner ◽  
Pituitary Adenylate Cyclase

The aim of the present study was to investigate the action of pituitary adenylate cyclase-activating polypeptide (PACAP) on ion transport in the guinea pig distal colon. Submucosal/mucosal segments from distal colon were mounted in Ussing flux chambers, and increases in short-circuit current (Isc) were used as an index of secretion. Serosal addition of PACAP-38 and PACAP-27 produced concentration-dependent (10(-10)-10(-6) M) increases in Isc. Furosemide and chloride-free solutions significantly reduced the PACAP-evoked responses. Tetrodotoxin (TTX) completely blocked PACAP-evoked responses. Atropine significantly reduced the PACAP-evoked responses but did not abolish the responses. The results suggest that PACAP evokes chloride secretion through cholinergic and noncholinergic neural mechanism. Vasoactive intestinal polypeptide (VIP), peptide histidine-isoleucine amide, and helodermin evoked Isc in a concentration-dependent manner. Atropine reduced but did not abolish the VIP- and related peptides-evoked responses. TTX also significantly decreased the responses to higher concentrations of VIP and related peptides but did not abolish the responses. The results suggest that VIP and related peptides act on both submucosal neurons and the epithelial cell itself. VIP tachyphylaxis significantly decreased PACAP-38- and PACAP-27-evoked responses. These results provide evidence that PACAP recognizes, in some part, VIP receptors in the submucosal neurons to evoke chloride secretion.

Endothelin stimulates chloride secretion across canine tracheal epithelium

1991 ◽  
Vol 261 (2) ◽  
pp. L188-L194 ◽  
Author(s):  
P. I. Plews ◽  
Z. A. Abdel-Malek ◽  
C. A. Doupnik ◽  
G. D. Leikauf
Keyword(s):  
Epithelial Cells ◽  
Short Circuit ◽  
Second Messengers ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Tracheal Epithelium ◽  
Membrane Phospholipids ◽  
Cl Secretion ◽  
Tracheal Epithelial Cells ◽  
Tracheal Epithelial

The endothelins (ET) are a group of isopeptides produced by a number of cells, including canine tracheal epithelial cells. Because these compounds are endogenous peptides that may activate eicosanoid metabolism, we investigated the effects of ET on Cl secretion in canine tracheal epithelium. Endothelin 1 (ET-1) was found to produce a dose-dependent change in short-circuit current (Isc) that increased slowly and reached a maximal value within 10-15 min. When isopeptides of ET were compared, 300 nM ET-1 and ET-2 produced comparable maximal increases in Isc, whereas ET-3 produced smaller changes in Isc (half-maximal concentrations of 2.2, 7.2, and 10.4 nM, respectively). Ionic substitution of Cl with nontransported anions, iodide and gluconate, reduced ET-1-induced changes in Isc. Furthermore, the response was inhibited by the NaCl cotransport inhibitor, furosemide. In paired tissues, ET-1 significantly increased mucosal net 36Cl flux without significant effect on 22Na flux. The increase in Isc induced by ET was diminished by pretreatment with indomethacin. The second messengers mediating the increase in Isc were investigated in cultured canine tracheal epithelial cells. ET-1 stimulated the release of [3H]arachidonate from membrane phospholipids, increased intracellular Ca2+ (occasionally producing oscillations), and increased adenosine 3',5'-cyclic monophosphate accumulation. The latter was diminished by indomethacin. Thus ET is a potent agonist of Cl secretion (with the isopeptides having the following potency: ET-1 greater than or equal to ET-2 greater than ET-3) and acts, in part, through a cyclooxygenase-dependent mechanism.

scholarly journals Enterotoxigenicity of Mature 45-Kilodalton and Processed 35-Kilodalton Forms of Hemagglutinin Protease Purified from a Cholera Toxin Gene-Negative Vibrio cholerae Non-O1, Non-O139 Strain

2006 ◽  
Vol 74 (5) ◽  
pp. 2937-2946 ◽  
Author(s):  
A. Ghosh ◽  
D. R. Saha ◽  
K. M. Hoque ◽  
M. Asakuna ◽  
S. Yamasaki ◽  
...  
Keyword(s):  
Cholera Toxin ◽  
Vibrio Cholerae ◽  
Hela Cells ◽  
Histopathological Examination ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Toxin Gene ◽  
Dependent Manner ◽  
A Cell

ABSTRACT Cholera toxin gene-negative Vibrio cholerae non-O1, non-O139 strain PL-21 is the etiologic agent of cholera-like syndrome. Hemagglutinin protease (HAP) is one of the major secretory proteins of PL-21. The mature 45-kDa and processed 35-kDa forms of HAP were purified in the presence and absence of EDTA from culture supernatants of PL-21. Enterotoxigenicities of both forms of HAP were tested in rabbit ileal loop (RIL), Ussing chamber, and tissue culture assays. The 35-kDa HAP showed hemorrhagic fluid response in a dose-dependent manner in the RIL assay. Histopathological examination of 20 μg of purified protease-treated rabbit ileum showed the presence of erythrocytes and neutrophils in the upper part of the villous lamina propria. Treatment with 40 μg of protease resulted in gross damage of the villous epithelium with inflammation, hemorrhage, and necrosis. The 35-kDa form of HAP, when added to the lumenal surface of rat ileum loaded in an Ussing chamber, showed a decrease in the intestinal short-circuit current and a cell rounding effect on HeLa cells. The mature 45-kDa form of HAP showed an increase in intestinal short-circuit current in an Ussing chamber and a cell distending effect on HeLa cells. These results show that HAP may play a role in the pathogenesis of PL-21.

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