Effects of histamine and histamine receptor antagonists on ion transport in rabbit descending colon

1984 ◽  
Vol 247 (4) ◽  
pp. G411-G418 ◽  
Author(s):  
R. D. McCabe ◽  
P. L. Smith
Keyword(s):  
Ion Transport ◽  
Receptor Antagonist ◽  
Prostaglandin E1 ◽  
Short Circuit ◽  
Bathing Solution ◽  
Ionophore A23187 ◽  
Dependent Manner ◽  
H2 Receptor Antagonist ◽  
Maximal Inhibition ◽  
Descending Colon

The effects of histamine on colonic ion transport were examined in in vitro preparations of rabbit descending colon. Serosal addition of histamine (10(-5) M) produced a transient increase in short-circuit current (Isc) and transepithelial conductance. The Isc response to histamine could be blocked by removing Cl from both bathing solutions, adding furosemide (10(-3) M) to the serosal bathing solution, adding indomethacin to the serosal and mucosal bathing solutions (10(-5) M), or removing Ca from the serosal bathing solution. In addition, the histamine-induced increase in Isc was inhibited in a dose-dependent manner by the H1-receptor antagonist diphenhydramine, with a maximal inhibition at 10(-4) M and a half-maximal inhibition at 3 X 10(-7) M. The H2-receptor antagonist cimetidine (10(-3) M) was without effect on the histamine response. Measurement of unidirectional Na, K, and Cl fluxes revealed that serosal addition of diphenhydramine (10(-3) M) reduced basal Isc due to a decrease in mucosal-to-serosal Na flux. Serosal addition of diphenhydramine (10(-3) M) also inhibited the increase in Isc produced by serosal addition of prostaglandin E1, 8-bromo-cAMP, cholera toxin, or the ionophore A23187. Measurement of unidirectional K and Cl fluxes revealed that prostaglandin E1 alone increased serosal-to-mucosal K and Cl fluxes and reduced the mucosal-to-serosal K flux, thereby increasing net K and Cl secretion. Serosal diphenhydramine (10(-3) M) abolished the changes in Cl fluxes produced by prostaglandin E1 and reduced the magnitude of the changes in K fluxes.(ABSTRACT TRUNCATED AT 250 WORDS)

Histamine stimulates ion transport by dog pancreatic duct epithelial cells through H1receptors

1998 ◽  
Vol 275 (1) ◽  
pp. G76-G84 ◽  
Author(s):  
Toan D. Nguyen ◽  
Charles N. Okolo ◽  
Mark W. Moody
Keyword(s):  
Epithelial Cells ◽  
Ion Transport ◽  
Receptor Antagonist ◽  
Pancreatic Duct ◽  
Direct Action ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Ussing Chambers

Histamine affects pancreatic secretion, but its direct action on ion transport by pancreatic duct epithelial cells (PDEC) has not been defined. We now characterize the secretory effects of histamine on cultured, well-differentiated, and nontransformed dog PDEC. Histamine stimulated, in a concentration-dependent manner (1–100 μM), a cellular125I−efflux that was inhibited by 500 μM 5-nitro-2-(3-phenylpropylamino)benzoic acid, 2.5 mM diphenylamine-2-carboxylate, and 500 μM DIDS and thus mediated through Ca2+-activated Cl− channels. Histamine-stimulated125I−efflux was 1) inhibited by 100 μM diphenhydramine, an H1receptor antagonist, 2) resistant to 1 mM cimetidine, an H2 receptor antagonist, 3) not reproduced by 1 mM dimaprit, an H2 agonist, and 4) inhibited by 50 μM 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid-AM, a Ca2+ chelator, suggesting that it was mediated through H1 receptors acting via increased cytosolic Ca2+. Histamine also stimulated a86Rb+efflux that was sensitive to 100 nM charybdotoxin and thus mediated through Ca2+-activated K+ channels. When PDEC monolayers were studied in Ussing chambers, a short-circuit current of 21.7 ± 3.1 μA/cm2 was stimulated by 100 μM histamine. This effect was inhibited by diphenhydramine but not cimetidine, was not reproduced with dimaprit, and was observed only after serosal addition of histamine, suggesting that it was mediated by basolateral H1 receptors on PDEC. In conclusion, histamine, acting through basolateral H1 receptors, activates both Ca2+-activated Cl− and K+ channels; in this manner, it may regulate PDEC secretion in normal or inflamed pancreas.

Effect of histamine on electrical and ion transport properties of tracheal epithelium

1977 ◽  
Vol 42 (5) ◽  
pp. 735-738 ◽  
Author(s):  
M. G. Marin ◽  
B. Davis ◽  
J. A. Nadel
Keyword(s):  
Ion Transport ◽  
Receptor Antagonist ◽  
Short Circuit ◽  
Electrical Potential ◽  
Ion Flux ◽  
Tracheal Epithelium ◽  
Electrical Potential Difference ◽  
H2 Receptor Antagonist ◽  
Water Secretion

Previously we showed that the active transport of Cl-toward and Na+ away from the tracheal lumen creates an electrical potential difference (lumen negative) across the canine tracheal epithelium in vitro. The present study examined the effect of histamine on the electrical properties and ion transport of the canine tracheal epithelium in vitro. In six pairs of membranes, under short-circuit conditions, histamine (10(-4) M) significantly increased the net flux toward the lumen of Cl- from 1.7 +- 0.5 SE to 2.4 +- 0.6 microneq/cm2-h and Na+ from -0.4 +- 0.3 to 0.2 +- 0.3 microneq/cm2-h. The response to histamine was inhibited by diphenhydramine (10(-6) M), an H1-receptor antagonist, but not by burimamide (10(-4) M), an H2-receptor antagonist. These results are consistent with the hypothesis that an H1-type receptor mediates the increase of ion flux toward the lumen due to histamine. Increased ion flux toward the lumen may mediate water secretion into the airway lumen and have important effects on the physical properties of the liquid through which the respiratory cilia beat.

Inhibition of midgut ion transport by allatotropin (Mas-AT) and Manduca FLRFamides in the tobacco hornworm Manduca sexta.

1998 ◽  
Vol 201 (22) ◽  
pp. 3067-3074 ◽  
Author(s):  
K Y Lee ◽  
F M Horodyski ◽  
M E Chamberlin
Keyword(s):  
Ion Transport ◽  
Manduca Sexta ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Dependent Manner ◽  
Additive Effects ◽  
Maximal Inhibition ◽  
Posterior Midgut ◽  
Active Ion Transport ◽  
Dose Dependent

Short-circuit current (Isc) across the posterior midgut of day 2 fifth-instar tobacco hornworms (Manduca sexta) is inhibited by Manduca allatotropin (Mas-AT) and two Manduca FLRFamides (F7G and F7D). Another FLRFamide, F10, and the related molluscan tetrapeptide FMRFamide elicited only a modest inhibition of Isc. Mas-AT, F7G and F7D inhibited the Isc in a dose-dependent manner. Maximal inhibition of Isc by Mas-AT was achieved at a concentration of 50 nmol l-1. At 100 nmol l-1, Mas-AT produced a significantly greater inhibition of Isc than did F7G and F7D. The inhibition caused by Mas-AT was reversed by removing the peptide. Furthermore, the action of Mas-AT could be blocked by preabsorption with its antiserum. When F7G or F7D was added after the Isc had been inhibited by Mas-AT, a further reduction in the Isc was observed. No additive effects were seen when F7G and F7D were added together. In comparison with the anterior and middle regions, the posterior section of the midgut was the most sensitive to these three peptides. The Isc of midguts dissected from feeding fourth instars was inhibited by Mas-AT, F7D and F7G, whereas the Isc of midguts dissected from pharate fifth instars or wandering fifth instars was virtually unaffected by these peptides. Active ion transport across the posterior midgut of the silk moths Hyalophora cecropia and Bombyx mori was unaffected by these peptides.

Measurement of short-circuit current and ion transport across the ileum

1964 ◽  
Vol 206 (3) ◽  
pp. 658-668 ◽  
Author(s):  
T. W. Clarkson ◽  
S. R. Toole
Keyword(s):  
Ion Transport ◽  
Sodium Transport ◽  
Chemical Potential ◽  
Short Circuit ◽  
Silver Ions ◽  
Short Circuit Current ◽  
Chloride Ions ◽  
Salt Transport ◽  
Complexing Agents ◽  
Bathing Solution

An apparatus is described which allowed control over both the electrical and chemical potential gradients across the isolated ileum of the rat and at the same time permitted the measurement of the transport of ions and water. Silver ions, released from the electrodes, affected ion transport. In the absence of complexing agents, the short-circuit current ( SCC) fell during the 60-min measurement period and was equal to the net sodium transport. With 10–3 m reduced glutathione in the bathing solution, the SCC was constant and equal to 94% of the sodium transport. With 10–4 m cysteine, the SCC was greatly increased. Sodium transport, also increased, was equal to 75% and chloride secretion to 20% of the SCC. A mechanism by which silver ions stimulate sodium transport, is proposed. Comparison of water and salt transport between open- and short-circuited tissues indicated that chloride ions were more effective in producing water movement when transported from mucosal to serosal solutions directly through the tissue (open circuit) rather than via the Ag/AgCl electrode system (short-circuit experiments).

Amiloride-sensitive and HCO3(-)-dependent ion transport activated by aldosterone and vasotocin in A6 cells

1995 ◽  
Vol 268 (3) ◽  
pp. C762-C770 ◽  
Author(s):  
Y. Doi ◽  
Y. Marunaka
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Arginine Vasotocin ◽  
Transient Increase ◽  
Epithelial Cell Line ◽  
Bathing Solution ◽  
Renal Epithelial Cell ◽  
Sustained Increase ◽  
In Cells

We studied the effects of aldosterone (Aldo) and arginine vasotocin (AVT) on ion transport of renal epithelial cell line (A6) by measuring short-circuit current (Isc). AVT induced a rapid, transient increase in Isc, followed by a decrease toward the baseline in cells untreated with Aldo. In cells treated with Aldo, Isc showed a biphasic response to AVT, i.e., both transient and sustained increases over 40 min after addition of AVT. The transient increase was composed only of amiloride-insensitive Isc regardless of Aldo treatment, whereas the sustained increase contained both amiloride-sensitive and amiloride-insensitive components. The main part of the amiloride-insensitive, sustained Isc depended on HCO3(-). In cells treated with Aldo for 1 day, removal of HCO3(-) in the bathing solution enhanced the amiloride-sensitive component and decreased the amiloride-insensitive one. These data suggest that 1) Aldo treatment is necessary for an AVT-induced sustained increase of Isc and 2) a HCO3(-)-dependent Isc mainly contributes to the sustained increase in amiloride-insensitive Isc.

Converging effects of a Bifidobacterium and Lactobacillus probiotic strain on mouse intestinal physiology

2014 ◽  
Vol 307 (2) ◽  
pp. G241-G247 ◽  
Author(s):  
Kevin W. Lomasney ◽  
John F. Cryan ◽  
Niall P. Hyland
Keyword(s):  
Ion Transport ◽  
Water Content ◽  
Short Circuit ◽  
Intestinal Transit ◽  
Current Response ◽  
Dependent Manner ◽  
Small Intestinal Transit ◽  
Ussing Chambers ◽  
Small Intestinal

Evidence has grown to support the efficacy of probiotics in the management of gastrointestinal disorders, many of which are associated with dysregulated fluid and electrolyte transport. A growing body of evidence now suggests that the host microbiota and probiotics can influence intestinal ion transport and that these effects often occur in a strain-dependent manner. In this study, we sought to investigate the effects of two therapeutically relevant organisms, Bifidobacterium infantis 35624 and Lactobacillus salivarius UCC118, on small intestinal transit, fecal output and water content, transepithelial resistance (TER), and colonic secretomotor function. Mice fed either strain displayed significantly reduced small intestinal transit in vivo, though neither strain influenced fecal pellet output or water content. Colon from mice fed both organisms displayed increased colonic TER, without a concomitant change in the gene expression of the tight junction proteins claudin 1 and occludin. However, L. salivarius UCC118 selectively inhibited neurally evoked ion secretion in tissues from animals fed this particular probiotic. Consistent with this finding, the neurotoxin tetrodotoxin (TTx) significantly inhibited the short-circuit current response induced by L. salivarius UCC118 following addition to colonic preparations in Ussing chambers. Responses to B. infantis 35624 also displayed sensitivity to TTx, although to a significantly lesser degree than L. salivarius UCC118. Both strains similarly inhibited cholinergic-induced ion transport after addition to Ussing chambers. Taken together, these data suggest that B. infantis 35624 and L. salivarius UCC118 may be indicated in disorders associated with increased small intestinal transit, and, in particular for L. salivarius UCC118, neurally mediated diarrhea.

Dantrolene and basal ileal sodium and chloride transport: involvement of calcium stores

1983 ◽  
Vol 245 (6) ◽  
pp. G780-G785
Author(s):  
M. Donowitz ◽  
S. Cusolito ◽  
L. Battisti ◽  
G. W. Sharp
Keyword(s):  
Ion Transport ◽  
Intracellular Calcium ◽  
Chloride Transport ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Calcium Stores ◽  
Ionophore A23187 ◽  
Rabbit Ileum ◽  
Intracellular Calcium Stores

The effect of dantrolene on active ion transport in rabbit ileum was determined using the Ussing chamber short-circuiting technique. Dantrolene prevents the release of calcium from intracellular stores in skeletal muscle and was used to probe the role of intracellular calcium stores in intestinal ion transport. A saturated solution of dantrolene (approx 25 microM) decreased ileal short-circuit current and potential difference, increased conductance and mucosal-to-serosal and net Na and Cl fluxes, but did not alter serosal-to-mucosal Na and Cl fluxes. The dantrolene stimulation of active Na and Cl absorption was specific since it did not alter glucose-dependent Na absorption, transport changes caused by Ca2+ ionophore A23187, or the increase in short-circuit current caused by dibutyryl cAMP or theophylline. These effects were associated with an increase in total ileal calcium content and a decreased rate of 45Ca2+ efflux without any change in 45Ca2+ influx from the serosal or mucosal surfaces. These findings are consistent with an effect of dantrolene to stimulate active ileal Na and Cl absorption by a mechanism involving lowered cytosol Ca2+ levels and compatible with trapping calcium in intracellular stores. It thus appears as if intracellular calcium stores have an important role in the control of basal ion transport in the intestine.

Hydrostatic pressure-regulated ion transport in bladder uroepithelium

2003 ◽  
Vol 285 (4) ◽  
pp. F651-F663 ◽  
Author(s):  
Edward C. Y. Wang ◽  
Jey-Myung Lee ◽  
John P. Johnson ◽  
Thomas R. Kleyman ◽  
Robert Bridges ◽  
...  
Keyword(s):  
Hydrostatic Pressure ◽  
Ion Transport ◽  
Volume Regulation ◽  
Short Circuit ◽  
Bathing Solution ◽  
Nonselective Cation Channel ◽  
Ussing Chambers ◽  
Mechanosensory Transduction ◽  
Electrolyte Homeostasis ◽  
Effect Of Hydrostatic Pressure

The effect of hydrostatic pressure on ion transport in the bladder uroepithelium was investigated. Isolated rabbit uroepithelium was mounted in modified Ussing chambers and mechanically stimulated by applying hydrostatic pressure across the mucosa. Increased hydrostatic pressure led to increased mucosal-to-serosal Na+ absorption across the uroepithelium via the amiloride-sensitive epithelial Na+ channel. In addition to this previously characterized pathway for Na+ absorption, hydrostatic pressure also induced the secretion of Cl– and K+ into the mucosal bathing solution under short-circuit conditions, which was confirmed by a net serosal-to-mucosal flux of 36Cl– and 86Rb+. K+ secretion was likely via a stretch-activated nonselective cation channel sensitive to 100 μM amiloride, 10 mM tetraethylammonium, 3 mM Ba2+, and 1 mM Gd3+. Hydrostatic pressure-induced ion transport in the uroepithelium may play important roles in electrolyte homeostasis, volume regulation, and mechanosensory transduction.

Intracellular Ca2+ and regulation of ion transport across rabbit Clara cells

1992 ◽  
Vol 263 (1) ◽  
pp. L122-L127
Author(s):  
M. R. Van Scott ◽  
A. M. Paradiso
Keyword(s):  
Epithelial Cells ◽  
Ion Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Airway Epithelial Cells ◽  
Clara Cell ◽  
Bathing Solution ◽  
Airway Epithelial ◽  
Clara Cells ◽  
Tracheal Cell

We investigated whether Ca2+ was involved in regulation of ion transport across rabbit distal airway epithelial cells by studying the effects that elevation of intracellular Ca2+ (Cai) had on the bioelectric properties of nonciliated bronchiolar (Clara) cell epithelia in culture. Exposure of Clara cells to 5 x 10(-7) M ionomycin increased Cai concentration and transepithelial short-circuit current (Isc). Changing extracellular Ca2+ concentration in the presence of ionomycin demonstrated that changes in Isc paralleled changes in Cai. Another ionophore, 4-bromo-A23187, also increased Cai and Isc. Ionomycin-induced changes in Isc were insensitive to amiloride and were inhibited greater than 50% by pretreating the cells with bumetanide or substituting gluconate for Cl- in the bathing solution. Bradykinin and carbachol, which increased Cai and caused an increase in Isc across tracheal cell cultures, had no effect on Cai or Isc in Clara cell preparations. These results support the hypothesis that changes in Cai are linked to regulation of Cl- secretion across bronchiolar epithelial cells, but physiological regulators of Cai in Clara cells remain to be defined.

scholarly journals Effects of collagen, ionophore A23187 and prostaglandin E1 on the phosphorylation of specific proteins in blood platelets

1979 ◽  
Vol 178 (2) ◽  
pp. 397-406 ◽  
Author(s):  
Richard J. Haslam ◽  
James A. Lynham ◽  
Joan E. B. Fox
Keyword(s):  
Cyclic Amp ◽  
Prostaglandin E1 ◽  
Blood Platelets ◽  
Short Circuit ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Human Platelets ◽  
Ionophore A23187 ◽  
Release Reaction ◽  
Specific Proteins

Human platelets that had been preincubated with 5-hydroxy[3H]tryptamine and [32P]Pi were stirred with various agents; the secretion of 5-hydroxy[3H]tryptamine from platelet granules and the radioactivity of platelet [32P]phosphopolypeptides separated by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis were then measured. Exposure of the platelets to collagen fibres or ionophore A23187 selectively increased the phosphorylation of polypeptides with apparent mol.wts. of 47000 (P47) and 20000 (P20) by approx. 3-fold, in association with the release of 5-hydroxy[3H]tryptamine. The 47000-mol.wt. phosphopolypeptide (P47) was clearly separated from platelet actin by the electrophoresis system used. Prostaglandin E1, which inhibits platelet function by increasing platelet cyclic AMP, decreased the phosphorylation of polypeptides caused by collagen as well as the release of 5-hydroxy[3H]tryptamine. Prostaglandin E1 also selectively increased the phosphorylation of distinct polypeptides with apparent mol.wts. of 24000 (P24) and 22000 (P22) by approx. 2-fold. As the phosphorylation reactions caused by collagen are probably mediated by an increase in Ca2+ concentration in the platelet cytosol and may have a role in the release reaction [Haslam & Lynham (1977) Biochem. Biophys. Res. Commun.77, 714–722; (1978) Thromb. Res.12, 619–628], we suggest that a cyclic AMP-dependent phosphorylation of the 24000- and/or 22000-mol.wt. polypeptides caused by prostaglandin E1 may initiate processes that decrease the Ca2+ concentration in the cytosol, so inhibiting both the Ca2+-dependent phosphorylation reactions and the release reaction. Treatment of platelets with prostaglandin E1 did not inhibit the increased phosphorylation of polypeptides with apparent mol.wts. of 47000 and 20000 (P47 and P20) caused by ionophore A23187, which may therefore short-circuit cyclic AMP-dependent mechanisms that decrease the Ca2+ concentration in the platelet cytosol. As prostaglandin E1 did inhibit the release of 5-hydroxy[3H]tryptamine by ionophore A23187, cyclic AMP may also inhibit the release reaction by additional mechanisms.

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