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.

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

1978 ◽  
Vol 44 (6) ◽  
pp. 900-904 ◽  
Author(s):  
M. G. Marin ◽  
M. M. Zaremba
Keyword(s):  
Electrical Properties ◽  
Ion Transport ◽  
Calcium Concentration ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Tracheal Epithelium ◽  
Electrical Potential Difference ◽  
Tracheal Lumen

Active transport of Cl- toward the tracheal lumen and Na+ away from the lumen creates an electrical potential difference across dog tracheal epithelium. This study examined in vitro the effect of varying calcium concentration in the bathing media on the ion transport and electrical properties of dog tracheal epithelium. In six pairs of epithelia, changing calcium concentration from 1.9 to 0 mM resulted in a significant decrease in electrical resistance, from 318 +/- 36 to 214 +/- 24 omega.cm2. Short-circuit current and net Cl- and Na+ fluxes measured under short-circuit conditions were not changed significantly. Changing calcium concentration from 1.9 to 10 mM resulted in no significant change from control in the electrical properties nor in net Cl- and Na+ fluxes (short-circuit conditions). Histamine (10(-4) M) produced a significantly smaller increase in short-circuit current in 0 than in 1.9 mM Ca2+ (+5 +/- 2 vs. +12 +/- 2 microamperemeter/cm2). However, electrical changes were not significantly different in 1 or 10 mM Ca2+. These results indicate that calcium lack increased permeability of tracheal epithelium and that the increase in short-circuit current due to histamine depended in part on calcium.

Effect of acetylcholine on Cl- and Na+ fluxes across dog tracheal epithelium in vitro

1976 ◽  
Vol 231 (5) ◽  
pp. 1546-1549 ◽  
Author(s):  
MG Marin ◽  
B Davis ◽  
JA Nadel
Keyword(s):  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Atropine Sulfate ◽  
Open Circuit ◽  
Ion Flux ◽  
Potential Difference ◽  
Tracheal Epithelium ◽  
Electrical Potential Difference

Electrical potential difference is generated across canine tracheal epithelium by active transport of Cl- toward and Na+ away from the lumen. The present study examines the effects of acetylcholine on short-circuit current, potential difference, resistance, and fluxes of 36Cl and 24Na measured across pieces of canine tracheal epithelium mounted in Ussing-type chambers. Under short-circuit conditions, acetylcholine (5 X 10(-5) M) increased significantly net ion flux toward the lumen of Cl- (n equals 7) from +1.7 +/- SE 0.5 TO +3.3 +/- SE 0.5 mueq/cm2 - h, and of Na+ (n equals 7) from -0.8 +/- SE 0.2 to +0.5 +/- SE 0.2 mueq/cm2 - h. Under open-circuit conditions, acetylcholine (5 X 10(-5) M) increased significantly the unidirectional flux of Cl- (n equals 6) toward the lumen from 4.7 +/- SE 1.3 to 5.9 +/- SE 1.4 mueq/cm2 - h, while the other measured fluxes did not change significantly, suggesting that net Cl- flux had increased toward the lumen. Atropine sulfate (10(-8) M) prevented the response to acetylcholine (5 X 10(-5) M). The increased ion flux due to acetylcholine may mediate water secretion into the airway lumen, and this secretion may have important effects on the physical properties of the liquid through which the respiratory cilia beat.

Effect of ethanol on ion transport and electrical properties of dog trachea in vitro

1983 ◽  
Vol 54 (5) ◽  
pp. 1335-1339 ◽  
Author(s):  
F. D. McCool ◽  
J. P. Zorn ◽  
M. G. Marin
Keyword(s):  
Electrical Properties ◽  
Ion Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Tracheal Epithelium ◽  
Electrical Potential Difference ◽  
Net Flux ◽  
Circuit Technique

We studied the effect of ethanol on the electrical and ion transport properties of dog tracheal epithelium using Ussing's short-circuit technique. There was a significant reduction of short-circuit current and electrical potential difference and a tendency of electrical resistance to increase in response to increasing concentrations of ethanol in the bathing solutions. Threshold changes in the electrical properties were noted at an ethanol concentration of 3.3 microliter/ml (260 mg/100 ml). Ethanol did not produce these changes in electrical properties when Cl- and Na+ were substituted in the bathing media with either choline or SO2-(4). In five paired tissue preparations, ethanol (13.3 microliters/ml) significantly reduced the net flux of Cl- toward the lumen from 2.68 +/- 0.62 to 1.00 +/- 0.69 (SE) mu eq X cm-2 X h-1, due primarily to a reduced unidirectional flux of Cl- from submucosa to lumen. These observations demonstrate that ethanol has an effect on the ion transport and electrical properties of dog tracheal epithelium at concentrations that may be of clinical relevance.

Electrophysiological properties of guinea pig tracheal epithelium determined by cable analysis

1993 ◽  
Vol 265 (1) ◽  
pp. L38-L44
Author(s):  
T. L. Croxton
Keyword(s):  
Guinea Pig ◽  
Ion Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Tracheal Epithelium ◽  
Sodium Absorption ◽  
Luminal Diameter ◽  
Cable Analysis

Electrophysiological characteristics of guinea pig tracheae were measured in vitro using an adaptation of cable analysis. This method allowed the repeated measurement of luminal diameter and epithelial electrical potential, resistance, and short-circuit current (Isc) during treatments known to affect smooth muscle contraction and epithelial ion transport. Stable values taken 3 h after mounting were as follows: diameter, 2.27 +/- 0.10 mm; potential, -28.3 +/- 2.3 mV; resistance, 327 +/- 30 omega.cm2; and Isc, 91.2 +/- 6.8 microA/cm2. These electrophysiological results are comparable to reported values for other species. However, the resistance and potential obtained in this study were larger than those previously reported for the guinea pig. Tracheal diameter was decreased 15% by methacholine and was increased 43% by subsequent isoproterenol treatment. Isoproterenol caused a small but significant increase in Isc when this quantity was normalized to tracheal length rather than to the apparent surface area. In contrast, apical amiloride decreased Isc by 51% and did not change diameter. These data validate this implementation of cable analysis, demonstrate that sodium absorption is the predominant mechanism of active ion transport by guinea pig tracheal epithelium, and indicate that this tissue has little capacity for stimulated chloride secretion.

OSMOTIC INHIBITION OF THE NATRIFERIC RESPONSE OF THE TOAD URINARY BLADDER TO VASOPRESSIN

1975 ◽  
Vol 67 (1) ◽  
pp. 119-125
Author(s):  
P. J. BENTLEY
Keyword(s):  
Urinary Bladder ◽  
Water Movement ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Toad Bladder ◽  
Toad Urinary Bladder ◽  
Electrical Potential Difference ◽  
Osmotic Gradient

SUMMARY The electrical potential difference and short-circuit current (scc, reflecting active transmural sodium transport) across the toad urinary bladder in vitro was unaffected by the presence of hypo-osmotic solutions bathing the mucosal (urinary) surface, providing that the transmural flow of water was small. Vasopressin increased the scc across the toad bladder (the natriferic response), but this stimulation was considerably reduced in the presence of a hypo-osmotic solution on the mucosal side, conditions under which water transfer across the membrane was also increased. This inhibition of the natriferic response did not depend on the direction of the water movement, for if the osmotic gradient was the opposite way to that which normally occurs, the response to vasopressin was still reduced. The natriferic response to cyclic AMP was also inhibited in the presence of an osmotic gradient. Aldosterone increased the scc and Na+ transport across the toad bladder but this response was not changed when an osmotic gradient was present. The physiological implications of these observations and the possible mechanisms involved are discussed.

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)

Effect of acetazolamide on sodium and chloride transport by in vitro rabbit ileum

1975 ◽  
Vol 228 (6) ◽  
pp. 1808-1814 ◽  
Author(s):  
HN Nellans ◽  
RA Frizzell ◽  
SG Schultz
Keyword(s):  
Cyclic Amp ◽  
Chloride Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Direct Interaction ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Membrane Component ◽  
Rabbit Ileum

Acetazolamide (8 mM) aboishes active Cl absorption and inhibits but does not abolish active Na absorption by stripped, short-circuited rabbit ileum. These effects are not accompanied by significant changes in the transmural electrical potential difference or short-circuit current. Studies of the undirectional influxes of Na andCl indicate that acetazolamide inhibits the neutral, coupled NaCl influx process at the mucosal membranes. This action appears to explain the observed effect of acetazolamide on active, transepithelial Na and Cl transport. Acetazolamide did not significantly inhibit either spontaneous or theophylline-induced Cl secretion by this preparation, suggesting that the theophylline-induced secretion may not simply be due tothe unmasking of a preexisting efflux process when the neutral influx mechanism is inhibited by theophylline. Finally, inhibition of the neutral NaCl influx process by acetazolamide does not appear to be attributable to an inhibition of endogenous HCO3production or an elevation in intracellular cyclic-AMP levels. Instead, it appearstheat the effect of acetazolamide is due to a direct interaction with a membrane component involved in the coupled influx process.

An Investigation of the Role of Possible Neural Mechanisms in Cholera Toxin-Induced Secretion in Rabbit Ileal Mucosa in Vitro

1989 ◽  
Vol 77 (2) ◽  
pp. 161-166 ◽  
Author(s):  
K. J. Moriarty ◽  
N. B. Higgs ◽  
M. Woodford ◽  
L. A. Turnberg
Keyword(s):  
Cholera Toxin ◽  
Fluid Transport ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Rabbit Ileum ◽  
Ileal Mucosa

1. Cholera toxin stimulates intestinal secretion in vitro by activation of mucosal adenylate cyclase. However, it has been proposed that cholera toxin promotes secretion in vivo mainly through an indirect mechanism involving enteric neural reflexes. 2. We examined this hypothesis further by studying the influence of neuronal blockade on cholera toxin-induced changes in fluid transport across rabbit ileum in vitro. Mucosa, stripped of muscle layers, was mounted in flux chambers and luminal application of crude cholera toxin (2 μg/ml) caused a delayed but sustained rise in the short-circuit current, electrical potential difference and Cl− secretion. Pretreatment with the nerve-blocking drug, tetrodotoxin (5 × 10−6 mol/l serosal side), failed to influence the secretory response to cholera toxin, and addition of tetrodotoxin at the peak response to cholera toxin also had no effect. 3. That tetrodotoxin could block neurally mediated secretagogues was confirmed by the demonstration that the electrical responses to neurotensin (10−7 mol/l and 10−8 mol/l) were blocked by tetrodotoxin (5 × 10−6 mol/l). Furthermore, the response to cholera toxin of segments of ileum, which included the myenteric, submucosal and mucosal nerve plexuses, was not inhibited by tetrodotoxin. 4. We conclude that cholera toxin-induced secretion in rabbit ileum in vitro is not mediated via a neurological mechanism.

Methylprednisolone increases absorptive capacity of rabbit ileum in vitro

1983 ◽  
Vol 245 (4) ◽  
pp. G562-G567 ◽  
Author(s):  
J. H. Sellin ◽  
R. C. DeSoignie
Keyword(s):  
Ion Transport ◽  
Absorptive Capacity ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Ion Flux ◽  
Rabbit Ileum ◽  
Transport Pathways ◽  
Na Pump ◽  
Intestinal Ion Transport

The effect of glucocorticoids on intestinal ion transport was studied in ileum in vitro from control and methylprednisolone (MP)-treated (40 mg im for 2 days) rabbits under the following conditions: a) basal rates of Na and Cl transport, b) the response to an individual absorptive stimulus (alanine, glucose, or epinephrine), and c) the response to a combination of the three absorptive stimuli. The results indicate that MP 1) increases basal absorption of Na and Cl and secretion of bicarbonate (as measured by residual ion flux), 2) does not alter the specific transport pathways stimulated by maximal doses of alanine, glucose, or epinephrine, but 3) significantly increases the absorptive capacity of ileum. After addition of combined alanine, glucose, and epinephrine, MP-treated ileum absorbed 15.8 mueq X cm-2 X h-1 Na (vs. 6.6 in controls, P less than 0.001) and 9.5 mueq X cm-2 X h-1 Cl (vs. 4.1 in controls, P less than 0.005). Additionally MP did not alter the Na dependence of either the short-circuit current or Cl absorption found in controls, although there appears to be a portion of residual ion flux insensitive to epinephrine inhibition. These data suggest that the MP-induced increase in absorptive capacity is due to an increase in a postapical transport step, most probably the Na pump.

In vitro studies of sodium transport across the lower intestine of a desert parrot

1980 ◽  
Vol 239 (3) ◽  
pp. R285-R290
Author(s):  
E. Skadhauge ◽  
T. J. Dawson
Keyword(s):  
Short Circuit ◽  
Electrical Potential ◽  
Flux Ratio ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Na Transport ◽  
Salt Loading ◽  
Ussing Chambers ◽  
Lower Intestine

The lower intestine (coprodeum and colon) of the Australian parrot, the galah, was mounted in Ussing chambers. Short-circuit current (SCC), electrical potential difference (PD), and unidirectional fluxes of Na and Cl were measured in birds that were fed mixed seeds or were NaCl loaded. The net Na transport of both coprodeum and colon was nearly equal to the SCC, and the flux ratio for Cl was unity. In birds which received mixed seeds, average coprodeal Na transport was 7.8 mu eq . cm-2 . h-1, and PD was 19 mV. The Km for Na was 5.7 meq/l. In colon, Na transport was reduced by 67% and PD by 70%. The ratio between unidirectional Na and Cl fluxes in the serosa-mucosa direction was 0.7. Salt loading suppressed coprodeal, but increased colonic Na transport. The coprodeal and colonic SCC and NA transport of birds receiving mixed seeds were inhibited by amiloride on the mucosal side. Colonic SCC of NaCl-loaded birds was only slightly reduced by amiloride (by 17%), but stimulated by amino acids (by 18%).

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