Sugar-stimulated ion absorption is not different in seahare and vertebrate intestine

1988 ◽  
Vol 255 (4) ◽  
pp. R583-R590
Author(s):  
W. M. Moran ◽  
L. T. Garretson
Keyword(s):  
Small Intestine ◽  
Apical Membrane ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Histological Findings ◽  
Ion Absorption ◽  
Ion Substitution ◽  
Membrane Electrical Potential

We have reexamined the notion that sugars stimulate ion absorption differently in invertebrate and vertebrate intestine. In the seahare intestine, mucosal sugar presumably increases the rate of transcellular Na+ and Cl- absorption, whereas only transcellular Na+ absorption is increased in the vertebrate small intestine. Our data indicate that the seahare intestine responds to mucosal D-galactose like the vertebrate small intestine: namely, the apical membrane electrical potential difference depolarizes, the ratio of the mucosal to serosal membrane resistances decreases, and the short-circuit current (Isc) increases. Because mucosal substitution of tetramethylammonium for Na+ abolished the increased Isc, this stimulation resulted from an increase in rheogenic Na+ absorption. Unidirectional transepithelial Cl- fluxes indicate that mucosal D-galactose had no effect on the net Cl- flux under short-circuit conditions. Further, ion substitution experiments indicate that the apical membrane is K+ conductive rather than Cl- conductive as previously reported. These electrophysiological as well as parallel histological findings indicate that studies previously reported on the seahare intestine were in fact conducted on the esophagus.

ADRENAL STEROIDS AND THE ELECTRICAL POTENTIAL OF RAT SMALL INTESTINE IN VIVO

1971 ◽  
Vol 49 (3) ◽  
pp. 377-386 ◽  
Author(s):  
H. M. NOBLE ◽  
A. J. MATTY
Keyword(s):  
Small Intestine ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Adrenal Steroids ◽  
Rat Small Intestine ◽  
Intestinal Activity ◽  
A New Technique

SUMMARY Using a new technique for determining transmucosal electrical potential difference (p.d.) and short-circuit current (Isc.) in the rat small intestine in vivo it would appear that aldosterone had no direct effect on these parameters of intestinal activity. However, adrenalectomy decreased the Isc. while after adrenalectomy aldosterone and cortisol (hydrocortisone) restored the lowered independent and probably also the lowered dependent (hexose) Isc.

Effect of L-alanine and ouabain on membrane conductances and apical membrane potential in Aplysia intestine

1995 ◽  
Vol 268 (4) ◽  
pp. R1050-R1059 ◽  
Author(s):  
S. R. Gabbard ◽  
W. M. Moran
Keyword(s):  
Apical Membrane ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Electrical Potential ◽  
Membrane Conductance ◽  
Short Circuit Current ◽  
Electrical Potential Difference ◽  
Control Value ◽  
Na Pump ◽  
Proximal Intestine

The proximal intestine of Aplysia californica was employed to assess the effect of alanine absorption on apical membrane K+ conductance (GKa) and basolateral membrane conductance (Gb) and the role of the electrogenic Na(+)-K(+)-adenosinetriphosphatase (Na+ pump) in the repolarization of apical membrane electrical potential difference (Va) after alanine-induced depolarization. Addition of 50 mM L-alanine (isosmotic substitution for mannitol) to the apical superfusate depolarized Va, reduced the ratio of apical to basolateral membrane resistances (Ra/Rb), and stimulated short-circuit current (Isc). Following these initial events, Va repolarized, Ra/Rb increased, and there was a slight decline in Isc. Apical high-K+ artificial seawater revealed an alanine-induced increase in GKa. Washout of alanine from the apical solution increased Ra/Rb above the prealanine control value. Thus alanine absorption is accompanied by an increase in Gb. Basolateral 0.1 mM ouabain abolished alanine-stimulated Isc but had little effect on Va ( < 3 mV depolarization) either before or after exposure to alanine. The repolarization of Va was not affected in tissues superfused with 0.1 mM basolateral ouabain for approximately 3 min even though the alanine-stimulated increase in Isc was abolished. Therefore, the electrogenic Na+ pump contributes minimally to the repolarization of Va in sea hare intestine. The origin of the hyperpolarization of Va resides therefore, at least in part, in the increase in GKa, which restores the driving force for Na(+)-alanine cotransport and prevents K+ accumulation in the enterocytes.

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.

Active electrolyte transport in mammalian buccal mucosa

1988 ◽  
Vol 255 (3) ◽  
pp. G286-G291 ◽  
Author(s):  
R. C. Orlando ◽  
N. A. Tobey ◽  
V. J. Schreiner ◽  
R. D. Readling
Keyword(s):  
Buccal Mucosa ◽  
Short Circuit ◽  
Basolateral Membrane ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Electrolyte Transport ◽  
Electrical Potential Difference ◽  
Ussing Chambers ◽  
Net Fluxes

The transmural electrical potential difference (PD) was measured in vivo across the buccal mucosa of humans and experimental animals. Mean PD was -31 +/- 2 mV in humans, -34 +/- 2 mV in dogs, -39 +/- 2 mV in rabbits, and -18 +/- 1 mV in hamsters. The mechanisms responsible for this PD were explored in Ussing chambers using dog buccal mucosa. After equilibration, mean PD was -16 +/- 2 mV, short-circuit current (Isc) was 15 +/- 1 microA/cm2, and resistance was 1,090 +/- 100 omega.cm2, the latter indicating an electrically "tight" tissue. Fluxes of [14C]mannitol, a marker of paracellular permeability, varied directly with tissue conductance. The net fluxes of 22Na and 36Cl were +0.21 +/- 0.05 and -0.04 +/- 0.02 mueq/h.cm2, respectively, but only the Na+ flux differed significantly from zero. Isc was reduced by luminal amiloride, serosal ouabain, or by reducing luminal Na+ below 20 mM. This indicated that the Isc was determined primarily by active Na+ absorption and that Na+ traverses the apical membrane at least partly through amiloride-sensitive channels and exits across the basolateral membrane through Na+-K+-ATPase activity. We conclude that buccal mucosa is capable of active electrolyte transport and that this capacity contributes to generation of the buccal PD in vivo.

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.

Cl- secretion by cultured shark rectal gland cells. II. Effects of forskolin on cellular electrophysiology

1991 ◽  
Vol 260 (4) ◽  
pp. C824-C831 ◽  
Author(s):  
W. M. Moran ◽  
J. D. Valentich
Keyword(s):  
Apical Membrane ◽  
Basolateral Membrane ◽  
Electrical Potential ◽  
Ringer Solution ◽  
Rectal Gland ◽  
Electrical Potential Difference ◽  
Electrophysiological Properties ◽  
Shark Rectal Gland ◽  
Membrane Electrical Potential ◽  
Cl Conductance

Employing microelectrode techniques we have assessed the cellular electrophysiological properties of shark rectal gland (SRG) cells in primary culture. In the absence of secretagogues a 10-fold reduction in the Cl- concentration of the apical superfusate shark Ringer solution had little effect on either apical membrane electrical potential difference (Va) or fractional resistance (fRa), indicating little, if any, apical membrane Cl- conductance. Superfusing the basolateral surface with high-K+ shark Ringer solution (K+ increased 10-fold) depolarized the basolateral membrane electrical potential difference (Vb) by 43 mV, indicating that this barrier is largely K+ conductive. In addition, basolateral Ba2+ (5 mM) depolarized Vb by 12 mV and reduced fRa from 0.92 to 0.58, results consistent with a K(+)-conductive basolateral membrane in unstimulated SRG cells. Basolateral forskolin (10(-6) M) depolarized Va by 25 mV and caused a dramatic reduction in fRa from 0.97 to approximately 0.10. Under these conditions, a 10-fold decrease in apical superfusate Cl- concentration depolarized Va by 37 mV, revealing an adenosine 3',5'-cyclic monophosphate-induced apical membrane Cl- conductance. The time course of the forskolin-induced changes in Va and Vb suggests that the basolateral membrane K+ conductance increased and maintained the driving force for apical Cl- exit, as in other Cl(-)-secreting epithelia. These electrophysiological properties compare favorably with those of the perfused SRG tubule and indicate that SRG primary cultures are a suitable model for Cl(-)-secreting epithelia.

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.

INTERRELATIONSHIP OF THE EFFECTS OF ALDOSTERONE AND THYROID HORMONES ON SODIUM TRANSPORT AND ELECTRICAL PROPERTIES OF RAT COLON

1970 ◽  
Vol 48 (2) ◽  
pp. 189-197 ◽  
Author(s):  
C. J. EDMONDS ◽  
B. D. THOMPSON ◽  
JANE MARRIOTT
Keyword(s):  
Body Weight ◽  
Electrical Resistance ◽  
Actinomycin D ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Rat Colon ◽  
Electrical Potential Difference ◽  
Influx Rate ◽  
Descending Colon

SUMMARY Transmucosal electrical potential difference (p.d.), short-circuit current, electrical resistance and Na+ influx rate of the descending colon were similar in euthyroid and hypothyroid rats, the latter having been treated earlier with an ablation dose of 131I. However, in contrast to the considerable p.d. increase found in normal rats, little change of p.d. was found in hypothyroid rats when they were Na+ depleted or given an intravenous aldosterone infusion. A single small dose of tri-iodothyronine (T3) (1 μg/100g body weight) or a larger dose of thyroxine given to hypothyroid rats 10–16 h before aldosterone, restored the p.d. response to normal, although these doses did not influence the animal's oxygen consumption. Fasting for 3 days or giving actinomycin D (8 μg/100 g body weight) abolished the effect of T3 but this did not influence the action of aldosterone in euthyroid animals.

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.

Effect of furosemide on the electrical parameters of frog skin

1982 ◽  
Vol 243 (6) ◽  
pp. F581-F587 ◽  
Author(s):  
A. Corcia ◽  
S. R. Caplan
Keyword(s):  
Active Transport ◽  
Frog Skin ◽  
Short Circuit ◽  
Electrical Potential ◽  
Short Circuit Current ◽  
Relative Increase ◽  
Electrical Potential Difference ◽  
Electrical Parameters ◽  
Active Conductance ◽  
Solution Bathing

When added to the mucosal solution bathing isolated frog skin at concentrations ranging from 5 X 10(-4) to 3 X 10(-3) M, the diuretic furosemide increased both the active transport of sodium and the electrical potential difference across the tissue in a dose-dependent way. The same effect was observed in chloride-free solutions. Mucosal furosemide also decreased the passive unidirectional fluxes of chloride. We believe that as far as electrical parameters are concerned mucosal furosemide has a double effect in frog skin: it increases the active conductance to sodium across the mucosal membrane, thus increasing active transport, and decreases the passive permeability to chloride, thus altering the passive conductance of the skin. The relative increase in short-circuit current was, however, invariably greater than the increase of the active conductance, suggesting the influence of yet a third effect. The effect of mucosal furosemide on active sodium transport was blocked by amiloride (5 X 1-(-5) M) and was independent of vasopressin. Qualitatively the effect was similar to the effect produced by triphenylmethylphosphonium ion.

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