scholarly journals Ion Transport in Isolated Rabbit Ileum

1964 ◽  
Vol 48 (2) ◽  
pp. 375-378 ◽  
Author(s):  
Stanley G. Schultz ◽  
Ralph Zalusky ◽  
Arthur E. Gass
Keyword(s):  
Ion Transport ◽  
Potential Gradient ◽  
Electrochemical Potential ◽  
Solvent Drag ◽  
Rabbit Ileum ◽  
Exchange Diffusion ◽  
Cl Transport ◽  
Ionic Conductances ◽  
Total Tissue

Unidirectional Cl fluxes across in vitro segments of rabbit ileum have been determined both in the absence and in the presence of an electrochemical potential gradient. The results indicate that Cl transport in this preparation can be attributed to purely passive forces uninfluenced by solvent drag or exchange diffusion. Furthermore, on the basis of this and previous studies, it has been demonstrated that the sum of the partial ionic conductances of Na and Cl accounts for at least 90 per cent of the total tissue conductance.

scholarly journals Sodium chloride transport by rabbit gallbladder. Direct evidence for a coupled NaCl influx process.

1975 ◽  
Vol 65 (6) ◽  
pp. 769-795 ◽  
Author(s):  
R A Frizzell ◽  
M C Dugas ◽  
S G Schultz
Keyword(s):  
Chloride Transport ◽  
Electrical Potential ◽  
Potential Gradient ◽  
Adenosine Monophosphate ◽  
Electrochemical Potential ◽  
Rabbit Ileum ◽  
Nacl Transport ◽  
Basolateral Membranes ◽  
Rabbit Gallbladder

The results of the present study that NaCl transport by in vitro rabbit gallbladder must be a consequence of a neutral coupled carrier-mediated mechanism that ultimately results in the active absorption of both ions; pure electrical coupling between the movements of Na and Cl can be excluded on the grounds of electrphysiologic considerations. Studies on the unidirectional influxes of Na and Cl have localized the site of this coupled mechanism to the mucosal membranes. Studies on the intracellular ion concentrations and the intracellular electrical potential are consistent with the notion that (a) the coupled NaCl influx process results in the movement of Cl from the mucosal solution into the cell against an apparent electrochemical potential difference; (b) the energy for the uphill movement of Cl is derived from the Na gradient across the mucosal membrane which is maintained by an active Na extrusion mechanism located at the basolateral membranes; and (c) Cl exit from the cell across the basolateral membranes is directed down an electrochemical potential gradient and may be diffusional. Finally, as for the case of rabbit ileum, the coupled NaCl influx process is inhibited by elevated intracellular levels of cyclic 3',5'-adenosine monophosphate. A working model for transcellular and paracellular NaCl transport by in vitro rabbit gallbladder is proposed.

scholarly journals Effects of exogenous and endogenous opiate compounds on ion transport in rabbit ileum in vitro

1978 ◽  
Vol 74 (5) ◽  
pp. 1081 ◽  
Author(s):  
L.C. Racusen ◽  
H.J. Binder ◽  
J.W. Dobbins
Keyword(s):  
Ion Transport ◽  
Rabbit Ileum ◽  
Endogenous Opiate

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.

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.

Effects of Berberine on Basal and Secretagogue-Modified Ion Transport in the Rabbit Ileum in Vitro

1987 ◽  
Vol 6 (6) ◽  
pp. 953-960 ◽  
Author(s):  
Stefano Guandalini ◽  
Alessio Fasano ◽  
Maurizio Migliavacca ◽  
Giuseppe Marchesano ◽  
Anna Ferola ◽  
...  
Keyword(s):  
Ion Transport ◽  
Rabbit Ileum

Effect of tetrodotoxin on cholinergic agonist-mediated colonic electrolyte transport

1983 ◽  
Vol 244 (4) ◽  
pp. G386-G391 ◽  
Author(s):  
T. W. Zimmerman ◽  
H. J. Binder
Keyword(s):  
Ion Transport ◽  
Electrolyte Transport ◽  
Rat Colon ◽  
Sodium Absorption ◽  
Muscarinic Agonist ◽  
Muscarinic Agonists ◽  
Rabbit Ileum ◽  
Cholinergic Agonist ◽  
Nicotinic Agonists

Muscarinic cholinergic agonists stimulate electrolyte secretion in the intestine; nicotinic agonists augment absorption. Recent studies in rabbit ileum suggest that nicotinic but not muscarinic agonists act via an intermediary neurotransmitter. These in vitro studies in rat colon were performed to determine whether tetrodotoxin (TTX), a potent neurotoxin, inhibits cholinergic agonist-induced changes in electrolyte transport. TTX did not significantly alter basal ion transport or the ion transport changes produced by either theophylline or bethanechol, a muscarinic agonist. At a concentration of 1 mM carbachol, a mixed muscarinic-nicotinic agonist, had no apparent effect on ion transport but in the presence of TTX significantly decreased net sodium absorption, similar to the effect produced by 1 microM carbachol alone. These results are consistent with the concept that in low concentrations carbachol acts predominantly as a muscarinic agonist; in high concentrations carbachol exhibits both muscarinic and nicotinic properties that are equivalent. We conclude that muscarinic agonists alter electrolyte transport by acting directly on the enterocyte and that nicotinic agonists act indirectly by stimulating the release of an intermediary neurotransmitter.

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.

Sign in / Sign up

Export Citation Format

Share Document