alpha 2-Adrenergic receptor regulation of ion transport in rabbit ileum

1982 ◽  
Vol 242 (3) ◽  
pp. G237-G242 ◽  
Author(s):  
E. B. Chang ◽  
M. Field ◽  
R. J. Miller
Keyword(s):  
Ion Transport ◽  
Adrenergic Receptor ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Maximal Effect ◽  
Rabbit Ileum ◽  
Ileal Mucosa ◽  
Receptor System ◽  
Alpha Adrenergic Receptors

Catecholamines are known to decrease short-circuit current (Isc), stimulate NaCl absorption, and inhibit HCO3 secretion in rabbit ileal mucosa in vitro. These effects appear to be mediated by alpha-adrenergic receptors because they are partially blocked by phentolamine and not by propranolol. To further characterize this receptor system, we determined the interactions of epinephrine (Epi) with alpha-subtype-selective antagonists. Prazosin (PZ), a specific alpha 1-antagonist, did not alter the Epi dose-response curve at concentrations up to 10(-5) M. Yohimbine (YO), a specific alpha 2-antagonist, completely inhibited the Epi effect on Isc. At 10(-5) M, YO increased by 70-fold the concentration of Epi required to produce a half-maximal effect (ED50; from 1.4 X 10(-7) M to 10(-5) M). YO and PZ by themselves had no significant effect on Isc in concentrations up to 10(-5) M. Clonidine, a specific alpha 2-agonist, decreased Isc with an ED50 similar to that of Epi; its effect was blocked by YO but not by PZ. Two alpha 1-selective agonists, methoxamine and phenylephrine, only caused a decrease in Isc in doses greater than 10(-5) M. This effect was reversed by YO but not by PZ. The effects of YO and PZ on Epi-modified Cl fluxes were also determined. YO completely aborted the effects of Epi on net Cl flux. No significant effects were seen with PZ. We conclude that the effects of Epi on ileal ion transport are mediated by a specific alpha 2-adrenergic receptor present in ileal mucosa and that no physiologic alpha 1-receptor function can be demonstrated.

Regulation of ion transport in porcine gallbladder: effects of VIP and norepinephrine

1989 ◽  
Vol 257 (1) ◽  
pp. C52-C57 ◽  
Author(s):  
S. M. O'Grady ◽  
P. J. Wolters ◽  
K. Hildebrand ◽  
D. R. Brown
Keyword(s):  
Receptor Antagonist ◽  
Adrenergic Receptor ◽  
Sulfonic Acid ◽  
Short Circuit ◽  
Fold Increase ◽  
Short Circuit Current ◽  
Maximal Effect ◽  
Camp Content ◽  
Flux Measurements

The objective of this study was to investigate the effects of vasoactive intestinal peptide (VIP) and norepinephrine (NE) on Na and Cl transport across the isolated porcine gallbladder. Serosal addition of either VIP or secretin increased the short-circuit current (Isc). The half-maximal effect for VIP was 84.3 nM. The effect of VIP was mimicked by 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP). Replacement of Cl with gluconate nearly abolished the effect of 8-BrcAMP on Isc, whereas HCO3 replacement with N-2-hydroxyethylpiperazine-N'-2-ethane-sulfonic acid buffer had no effect. Transepithelial flux measurements indicated that 8-BrcAMP stimulates net Cl secretion and inhibits Na absorption. Norepinephrine inhibits VIP-stimulated changes in Isc as well as the basal Isc. NE does not, however, reverse the effects of 8-BrcAMP on Isc. The effects of NE are antagonized by yohimbine (alpha 2-adrenergic receptor antagonist) but not prazosin (an alpha 1-adrenergic receptor antagonist). VIP causes a 2.5-fold increase in cAMP content in the gallbladder epithelium. This increase is blocked by NE. Serosal tetrodotoxin did not inhibit the peptide effects, indicating that VIP receptors are localized on the epithelium. Depolarization of submucosal nerves with veratrine inhibited the basal Isc and was reversible with yohimbine. This result indicated that sympathetic nerve pathways regulate Na and Cl absorption in vitro.

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.

cGMP modulation of ileal ion transport: in vitro effects of Escherichia coli heat-stable enterotoxin

1982 ◽  
Vol 243 (1) ◽  
pp. G36-G41 ◽  
Author(s):  
S. Guandalini ◽  
M. C. Rao ◽  
P. L. Smith ◽  
M. Field
Keyword(s):  
Escherichia Coli ◽  
Ion Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Rabbit Ileum ◽  
Heat Stable ◽  
Transport Effects ◽  
In Vitro Effects ◽  
Nonadditive Effects

Diarrheagenic strains of Escherichia coli have been shown to produce a heat-stable enterotoxin (ST) that simulates guanylate cyclase, increases short-circuit current (Isc), and inhibits active Cl absorption in the intestine. In rabbit ileum, the ion transport effects are smaller than those produced by cAMP-related agonists. Because ST may be a selective cGMP agonist, we further explored its mode of action in rabbit ileum. ST inhibits net Na and net Cl absorption. ST also inhibits the same fraction of Cl influx across the brush border that theophylline inhibits. At maximal doses, ST and 8-bromo-cGMP (8-Br-cGMP) had nearly equal, nonadditive effects of Isc that were about 66% of that produced by 8-Br-cAMP. ST increased mucosal cGMP concentration 16-fold, whereas epinephrine, an inhibitor of secretion, increased cGMP concentration by only 30%. This is insufficient to alter ion transport because doses of ST that increased cGMP concentration by 100% failed to alter Cl fluxes. Furthermore, epinephrine did not increase cGMP concentration in isolated enterocytes. We conclude that 1) cGMP mediates ST effects on ion transport, and 2) although ST and cAMP-related agonists have the same antiabsorptive effects, ST is less effective in stimulating electrogenic Cl secretion.

Endogenous norepinephrine release induced by tyramine modulates intestinal ion transport

1981 ◽  
Vol 241 (3) ◽  
pp. G264-G269 ◽  
Author(s):  
E. J. Tapper ◽  
A. S. Bloom ◽  
D. L. Lewand
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Current Response ◽  
Na Transport ◽  
Rabbit Ileum ◽  
Nacl Transport ◽  
6 Hydroxydopamine ◽  
Intestinal Ion Transport

To study the effects of endogenous norepinephrine on intestinal ion transport, we tested the actions of an indirect sympathomimetic agent, tyramine, on electrolyte fluxes in the short-circuited rabbit ileum in vitro. Tyramine (10(-5) M) alone had no effect on short-circuit current or Na transport but increased Cl absorption. Tyramine decreased the short-circuit current, stimulated both Na and Cl absorption, and increased tissue conductance when its breakdown by endogenous monoamine oxidase enzymes was inhibited by pretreatment with pargyline (10(-4) M). Pargyline alone had no effect on short-circuit current and NaCl transport. The effect of norepinephrine on NaCl transport was inhibited by the alpha-adrenergic receptor antagonist, phentolamine (10(-7) M). This response was also prevented when animals were chemically sympathectomized with 6-hydroxydopamine. Although sympathectomy decreased measurable tissue norepinephrine by 80%, it did not alter basal short-circuit current, Na and Cl absorption, and the short-circuit current response to glucose-stimulated Na transport and to exogenous norepinephrine. Thus, a pool of norepinephrine in intestinal adrenergic neurons released by tyramine affects intestinal ion transport but does not alter basal ion transport. These data suggest close neuropharmacologic similarities between the adrenergic nervous system in the intestine and other organs.

Avian cecum: role of glucose and volatile fatty acids in transepithelial ion transport

1991 ◽  
Vol 260 (5) ◽  
pp. G703-G710 ◽  
Author(s):  
B. R. Grubb
Keyword(s):  
Fatty Acids ◽  
Ion Transport ◽  
Volatile Fatty Acids ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Serosal Side ◽  
Na Transport ◽  
Cl Secretion ◽  
Mucosal Side

In the fowl cecum in vitro, the influence of glucose and the three most prevalent naturally occurring volatile fatty acids (acetate, propionate, butyrate) on short-circuit current (Isc), electrical resistance, and transport of Na and Cl was determined. When glucose, acetate, or butyrate was present, ion transport was characterized by electrogenic Na absorption, greater than 65% of which was amiloride inhibitable, and Cl secretion, which also was electrogenic. Isc could be completely accounted for by net fluxes of Na and Cl. When glucose, acetate, or butyrate (10 mM both sides) was included in the incubation medium, cecal tissue maintained its Isc and a constant rate of net Na absorption and Cl secretion for a 5-h period. When no substrate was present or propionate was included in the medium, a marked fall in Isc and net Na and Cl fluxes was seen. Glucose caused an increase in Isc when added only to the serosal side. As 3-O-methylglucose (not metabolized) was not effective in stimulating Isc of the cecum (serosal or mucosal addition), it appeared that glucose increased Isc by acting as an energy substrate for active Na transport. Acetate and butyrate appeared to be equally effective in stimulating Na transport and Isc when placed on either side of the membrane. When the preparation was supplied with glucose (serosal side) and acetate was added to the mucosal side, no further stimulation of Isc occurred. Thus it appeared that acetate and butyrate were acting as substrates for active Na transport rather than stimulating Na transport by some other mechanism such as a cotransport with Na.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Intestinal mucosal cyclic GMP: regulation and relation to ion transport

1976 ◽  
Vol 231 (1) ◽  
pp. 275-282 ◽  
Author(s):  
TA Brasitus ◽  
M Field ◽  
DV Kimberg
Keyword(s):  
Causal Relationship ◽  
Cyclic Gmp ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Ileal Mucosa ◽  
Muscarinic Cholinergic Receptors ◽  
Cholecystokinin Octapeptide ◽  
Muscarinic Cholinergic ◽  
Stimulation Of

Stimulation of alpha-adrenergic and muscarinic cholinergic receptors in rabbit ileal mucosa in vitro produced 5- to 15-fold increases in cyclic GMP (cGMP) concentration that were maximal within 2 min and gone within 30 min. Cholecystokinin octapeptide and insulin caused similar increases in cGMP. None of these agents affected cAMP. The epinephrine-induced increase in cGMP was blocked by atropine at 100 but not at 1 muM concentration. Epinephrine stimulates active NaCl absorption and decreases short-circuit current (SCC) in vitro, the latter effect due to inhibition of HCO3 secretion. Atropine (100 muM) blocked the former but not the latter effect of epinephrine. In vitro additions of several concentrations of cGMP and 8-bromo-cGMP did not decrease SCC or alter Na fluxes. Thus, changes in cGMP concentration have been directly correlated with changes in active absorption of NaCl, but a causal relationship has not been proven.

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.

Bioelectric properties and ion flow across excised human bronchi

1984 ◽  
Vol 56 (4) ◽  
pp. 868-877 ◽  
Author(s):  
M. Knowles ◽  
G. Murray ◽  
J. Shallal ◽  
F. Askin ◽  
V. Ranga ◽  
...  
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Maximal Effect ◽  
Na Transport ◽  
Adrenergic Agents ◽  
Ion Flow ◽  
Cl Secretion ◽  
Active Ion Transport ◽  
Human Bronchi

Bioelectric properties and ion transport of excised human segmental/subsegmental bronchi were measured in specimens from 40 patients. Transepithelial electric potential difference (PD), short-circuit current (Isc), and conductance (G), averaged 5.8 mV (lumen negative), 51 microA X cm-2, and 9 mS X cm-2, respectively. Na+ was absorbed from lumen to interstitium under open- and short-circuit conditions. Cl- flows were symmetrical under short-circuit conditions. Isc was abolished by 10(-4) M ouabain. Amiloride inhibited Isc (the concentration necessary to achieve 50% of the maximal effect = 7 X 10(-7) M) and abolished net Na+ transport. PD and Isc were not reduced to zero by amiloride because a net Cl- secretion was induced that reflected a reduction in Cl- flow in the absorptive direction (Jm----sCl-). Acetylcholine (10(-4) M) induced an electrically silent, matched flow of Na+ (1.7 mueq X cm-1 X h-1) and Cl- (1.9 mueq X cm-12 X h-1) toward the lumen. This response was blocked by atropine. Phenylephrine (10(-5) M) did not affect bioelectric properties or unidirectional ion flows, whereas isoproterenol (10(-5) M) induced a small increase in Isc (10%) without changing net ion flows significantly. We conclude that 1) Na+ absorption is the major active ion transport across excised human bronchi, 2) Na+ absorption is both amiloride and ouabain sensitive, 3) Cl- secretion can be induced by inhibition of the entry of luminal Na+ into the epithelia, and 4) cholinergic more than adrenergic agents modulate basal ion flow, probably by affecting gland output.

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