Absorption of glucose by lamb proximal colon measured during early postnatal development

1982 ◽  
Vol 98 (1) ◽  
pp. 161-165 ◽  
Author(s):  
M. W. Smith ◽  
P. S. James
Keyword(s):  
Glucose Transport ◽  
Time Course ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Proximal Colon ◽  
Postnatal Life ◽  
Early Postnatal Development ◽  
Rumen Development ◽  
Active Transport System

SUMMARYPieces of proximal colon taken from lambs during the first 2 weeks of postnatal life were incubated in vitro for measurement of short-circuit current and unidirectional glucose fluxes.The short-circuit current of colons taken from newborn and 1-day-old lambs was increased significantly in the presence of 5 mM D-glucose. This is taken as evidence for the presence of an active transport system for monosaccharides in this tissue. No such effect was seen using colons taken from 2-week-old lambs.Direct measurement of glucose transport showed a net absorption to take place across the proximal colon of newborn and 1-day-old lambs. There was no net movement across colons taken from lambs aged 1 week and over. Essentially similar results were obtained when measuring the amount of glucose influx inhibited by 10−5 M phloridzin.Colonic decline of glucose transport follows a time course different from that reported previously for the small intestine. It probably arises from rapid maturation of the colonic mucosa postnatally rather than from any gradual absence of substrate occurring during rumen development.

Sodium transport by lamb proximal colon measured during early postnatal development

1982 ◽  
Vol 98 (1) ◽  
pp. 155-159 ◽  
Author(s):  
M. W. Smith ◽  
P. S. James
Keyword(s):  
Postnatal Development ◽  
Sodium Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Proximal Colon ◽  
Early Postnatal Development ◽  
The Third ◽  
Electrolyte Absorption ◽  
Chloride Absorption

SUMMARYProximal colons taken from lambs up to 3 weeks after birth were shown to transport both sodium and chloride from lumen to blood when incubated in vitro.Sodium transport fell into three phases during postnatal development. The first covered the period from birth to 3 days of age when sodium transport was high and equal to that calculated from measurement of short-circuit current. The second was seen in 5- and 7-day-old lambs where the short-circuit current was low and the net transport of sodium was negligible. The third was seen in 2-3-week-old lambs where sodium transport was high, but the short-circuit current was low.Chloride absorption by colons taken from 1-day-old lambs appeared to be in exchange for an anion, possibly bicarbonate. Chloride absorption by colons taken from 3-week-old lambs appeared to be electrogenie or coupled directly to the transport of sodium.A possible explanation for the failure of electrolyte absorption by colons taken from 5- and 7-day-old lambs is discussed.

NaCl transport across equine proximal colon and the effect of endogenous prostanoids

1990 ◽  
Vol 259 (1) ◽  
pp. G62-G69 ◽  
Author(s):  
L. L. Clarke ◽  
R. A. Argenzio
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Proximal Colon ◽  
Nacl Transport ◽  
Apparent Lack ◽  
Ussing Chambers ◽  
Cl Secretion

In contrast to in vivo findings, the equine proximal colon fails to demonstrate significant net absorption of Na+ and Cl- under in vitro conditions. The present study was undertaken to determine if endogenous prostanoids are responsible for this apparent lack of ion transport. Proximal colonic tissues from ponies were preincubated in either normal Ringer solution or in Ringer containing 1 microM indomethacin and studied in Ussing chambers containing these solutions. Untreated colonic mucosa demonstrated negligible Na(+)-Cl- absorption in the basal state. In contrast, indomethacin-treated colon significantly absorbed Na+ and Cl-, primarily as the result of an equivalent increase in the mucosal-to-serosal flux of these ions. Preincubation of proximal colon in 0.1 mM ibuprofen-treated Ringer yielded similar results. Treatment of indomethacin colon with 1 mM mucosal amiloride eliminated net Na(+)-Cl- absorption without affecting the short-circuit current (Isc). The Isc in control tissue was significantly greater than in indomethacin-treated tissue and was reduced by 0.1 mM serosal furosemide. Serosal addition of 0.1 microM prostaglandin E2 or 10 mM serosal plus mucosal theophylline to indomethacin-treated tissues abolished net Na(+)-Cl- absorption and increased the Isc to levels indistinguishable from control. In contrast, control tissues were essentially unaffected by these secretagogues. These findings indicated that Na(+)-Cl- absorption in equine proximal colon was electroneutral (possibly involving Na(+)-H+ exchange) and that the tissue was capable of electrogenic Cl- secretion. However, under the in vitro conditions, basal ion transport was dominated by endogenous prostanoids that abolished Na(+)-Cl- absorption and elicited near-maximal electrogenic Cl- secretion.

Regulation of Na-Cl absorption in rabbit proximal colon in vitro

1987 ◽  
Vol 252 (1) ◽  
pp. G45-G51 ◽  
Author(s):  
J. H. Sellin ◽  
R. De Soignie
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Proximal Colon ◽  
Beta Agonist ◽  
Disulfonic Acid ◽  
Low Concentrations ◽  
Cotransport System ◽  
Net Flux

Ion transport in rabbit proximal colon (PC) in vitro is dominated by a Na-Cl cotransport system stimulated by epinephrine. To further characterize the regulation of Na-Cl transport, we tested the effects of specific adrenergic agonists on ion fluxes under short-circuit conditions. Additionally, we tested the effects of the transport inhibitors bumetanide, furosemide, and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS). Basal Na and Cl absorption were essentially nil [Na net flux (JNanet) = 0.3 +/- 0.4, and Cl net flux (JClnet) = -0.5 +/- 0.5 mu eq X cm-2 X h-1, means +/- SE]. The alpha 2-agonist clonidine significantly increased net Na and Cl absorption (delta JNanet = 3.0 +/- 0.6 mu eq X cm-2 X h-1, delta JClnet = 2.0 +/- 0.4 mu eq X cm-2 X h-1) with a minimal change in short-circuit current (delta Isc = 0.1 +/- 0.1 mu eq X cm-2 X h-1). The alpha 1-agonist phenylephrine and the beta-agonist isoproterenol did not alter ion transport. The alpha 2-blocker yohimbine (YOH) had a complex, concentration-dependent effect. At low concentrations (10(-6)-10(-8) M) YOH effectively inhibited epinephrine-stimulated cotransport. Compared with 10(-8)M YOH, 10(-6) YOH blocked 90% of the epinephrine-induced increases in Na and Cl absorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Contrasting effects of PGE2 and PGD2: ion transport in the canine proximal colon

1991 ◽  
Vol 260 (3) ◽  
pp. G481-G488 ◽  
Author(s):  
C. M. Keenan ◽  
P. K. Rangachari
Keyword(s):  
Prostaglandin E2 ◽  
Early Phase ◽  
Marked Reduction ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Proximal Colon ◽  
Colonic Epithelium ◽  
Specific Antagonist ◽  
Later Phase

Our earlier study [Am. J. Physiol. 256 (Gastrointest. Liver Physiol. 19): G673-G679, 1989] showed that the isomers prostaglandin E2 and D2 (PGE2 and PGD2) had contrasting effects on the canine proximal colonic epithelium in vitro. Whereas PGE2 produced sharp increases in short-circuit current (Isc), PGD2 rapidly reversed these changes. We report here that PGD2 reversed increases in Isc produced by other agonists (forskolin, carbachol) and was thus not a specific antagonist to PGE2. The transient increase in Isc and conductance produced by PGE2 were accompanied by alterations in Cl- but not Na+ fluxes. These were partitioned into early and late phases. In the early phase, net Cl- flux (JCl-net) decreased due to a reduction in Cl- mucosal to serosal flux (JCl-m----s) and increases in JCl-s----m. In the later phase, these changes appeared to revert to prestimulation values. Because forskolin produced more sustained increases in Isc, we used it as an agonist to define the effects of PGD2 on ion fluxes. Forskolin produced a marked reduction in JCl-net due to a decrease in JCl-m----s and an increase in JCl-s----m. PGD2 not only reversed the increases in Isc and conductance produced but also reversed the changes in Cl- flux.

Steroids alter ion transport and absorptive capacity in proximal and distal colon

1985 ◽  
Vol 249 (1) ◽  
pp. G113-G119 ◽  
Author(s):  
J. H. Sellin ◽  
R. C. DeSoignie
Keyword(s):  
Ion Transport ◽  
Absorptive Capacity ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Proximal Colon ◽  
High Rate ◽  
Transport Parameters ◽  
In Vitro Effects

Steroids are potent absorbagogues, increasing Na and fluid absorption in a variety of epithelia. This study characterizes the in vitro effects of pharmacological doses of gluco- and mineralocorticoids on transport parameters of rabbit proximal and distal colon. Treatment with methylprednisolone (MP, 40 mg im for 2 days) and desoxycortone acetate (DOCA, 12.5 mg im for 3 days) resulted in a significant increase in short-circuit current (Isc) in distal colon, suggesting an increase in basal Na absorption. Amiloride (10(-4) M) caused a significantly negative Isc in MP-treated tissue, demonstrating a steroid-induced, amiloride-insensitive electrogenic ion transport in distal colon. The effect of two absorbagogues, impermeant anions (SO4-Ringer) and amphotericin, were compared in control and steroid-treated distal colon. In controls, both absorbagogues increased Isc. Impermeant anions caused a rise in Isc in both MP and DOCA tissues, suggesting that the high rate of basal Na absorption had not caused a saturation of the Na pump. The steroid-treated colons, however, did not consistently respond to amphotericin. Amiloride inhibited the entire Isc in MP-treated distal colon that had been exposed to amphotericin; this suggested that amphotericin had not exerted its characteristic effect on the apical membrane of steroid-treated colon. In proximal colon, steroids did not alter basal rates of transport; however, epinephrine-induced Na-Cl absorption was significantly greater in MP-treated vs control (P less than 0.005). Steroids increase the absorptive capacity of both proximal and distal colon for Na, while increasing basal Na absorption only in the distal colon.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone-induced, amiloride-inhibitable short-circuit current in the avian ileum

1987 ◽  
Vol 253 (2) ◽  
pp. G211-G216
Author(s):  
B. R. Grubb ◽  
P. J. Bentley
Keyword(s):  
Time Course ◽  
Short Circuit ◽  
Electrical Potential ◽  
Intestinal Transport ◽  
Short Circuit Current ◽  
Na Channel ◽  
Electrical Potential Difference ◽  
Adaptation Mechanisms ◽  
Channel Blocking

Transmural electrical potential difference, short-circuit current (Isc), and resistance were measured in vitro in the intestines of chickens. In birds maintained on a low-Na diet, there was a rise in Isc in the ileum and the colon but not in the duodenum or jejunum. A substantial portion of this Isc could be inhibited by the Na channel-blocking drug, amiloride. The low-Na diet results in elevated plasma levels of aldosterone and the effects of the diet on intestinal transport could be mimicked by administration of this hormone. The time course of the effects of these two treatments on the ileum and colon were quite different, as a much longer exposure was needed to elicit maximal effects in the ileum than in the colon, possibly due to the presence of two types of adaptation mechanisms. The responses observed may reflect an adaptation of mechanisms for increasing Na transport from the intestine. The presence of such a mechanism in the vertebrate ileum has until recently been in doubt.

Dietary flavonol quercetin induces chloride secretion in rat colon

1998 ◽  
Vol 275 (5) ◽  
pp. G1166-G1172 ◽  
Author(s):  
Rainer Cermak ◽  
Ursula Föllmer ◽  
Siegfried Wolffram
Keyword(s):  
Short Circuit ◽  
Ussing Chamber ◽  
Phosphodiesterase Inhibitor ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Chloride Secretion ◽  
Proximal Colon ◽  
Rat Colon ◽  
Quercetin Glycoside

The aim of this study was to investigate the possible effects of the flavonol quercetin, the most abundant dietary flavonoid, on the intestinal mucosa. In vitro experiments were performed with various segments of the rat intestine, using the Ussing chamber technique. Quercetin increased the short-circuit current ( I sc) in the jejunum, ileum, and proximal and distal colon. Additional experiments were performed using preparations of the proximal colon. The maximum effective dose of quercetin was found to be ∼100 μM. The quercetin-induced increase in I sc was inhibited by the Cl− channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoic acid. Adding blockers of the Na+-K+-2Cl−cotransporter to the serosal compartment diminished the increase of I sc due to quercetin. Ion substitution and flux measurements indicated that the effect of quercetin was due to electrogenic Cl− and[Formula: see text] secretion. In contrast to the aglycone, the quercetin glycoside rutin had no effect. The effect of quercetin on I scwas additive to the I sc increase induced by forskolin, but the flavonoid diminished the I sc evoked by carbachol. The phosphodiesterase inhibitor theophylline blocked the effect of quercetin. Genistein, a related isoflavone, did not alter the I sc evoked by quercetin. These findings demonstrate that the dietary flavonol quercetin induces Cl−secretion and most likely [Formula: see text]secretion in rat small and large intestine. The effects are restricted to the flavonol aglycone.

Amiloride-sensitive salt and fluid absorption in small intestine of sodium-depleted rats

1985 ◽  
Vol 248 (1) ◽  
pp. G133-G141 ◽  
Author(s):  
P. C. Will ◽  
R. N. Cortright ◽  
R. G. Groseclose ◽  
U. Hopfer
Keyword(s):  
Small Intestine ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Proximal Colon ◽  
Salt Transport ◽  
Fluid Absorption ◽  
Major Pathway

Secondary hyperaldosteronism produced by Na+ depletion was associated with increases in salt and fluid absorption in both the small intestine and the distal colon but not in the cecum and the proximal colon. Because these changes had not been documented for the small intestine, this study focused on the regulation of this tissue. Increased NaCl and water absorption was expressed in vitro by increases in short-circuit current and transepithelial potential and in vivo by increased fluid absorption and a decreased luminal content of Na+ and water. For example, the short-circuit current in the ileum of Na+-depleted rats was 2-fold that of adrenalectomized and 1.3-fold that of adrenal-intact control animals. The short-circuit current was inhibitable 24 +/- 14% by micromolar concentrations of amiloride in Na+-deficient animals compared with 1 +/- 3% in control animals. Similarly, ileal fluid absorption in vivo was 2.3-fold higher in Na+-deficient relative to control animals. The additional fluid absorption was sensitive to 50 microM amiloride, whereas amiloride had no effect in control animals. Furthermore, the Na+ content of the chyme from the ileum of Na+-deficient animals was about half that of controls. These results suggest that mineralocorticoids can induce the amiloride-sensitive Na+ transporter in the small intestine and that this type of epithelial salt transport can become a major pathway for salt retention by the small intestine.

Na+-dependent H+ and Cl- transport in in vitro frog gastric mucosa

1980 ◽  
Vol 238 (5) ◽  
pp. G403-G413 ◽  
Author(s):  
T. E. Machen ◽  
W. L. McLennan
Keyword(s):  
Time Course ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Ringer Solution ◽  
Open Circuit ◽  
Cl Transport ◽  
Coupled Process ◽  
Separate System ◽  
Energy Dependent

Na+ dependency of H+ and Cl- transport in resting and stimulated gastric mucosae was investigated. We measured transepithelial potential difference (PD), short-circuit current (Isc), conductance, H+ secretion (JH), and unidirectional fluxes of 36Cl- (muscosal (m) to serosal (s), JClm leads to s and JCLs leads to m) during Isc conditions in Ussing-type chambers. Resting tissues: Na+-free serosal solution (choline replacement), but not mucosal, Ringer solution caused PD and Isc to decrease to zero with a time course identical to that observed with Cl--free solutions. Conductance also decreased by more than 50%. Isc = JCLs leads to m--JCLm leads to 8 = JClnet during control ([Na+] = 105 mM), and Na+-free conditions. When [Na+] = 50 mM (choline replacement) Isc (=JClnet) was reduced by approximately 25%; when K+ replaced Na+, Isc (=JClnet) was reduced by approximately 65%. The dependence of Isc on [Na+] (choline replacement) was sigmoidal indicating that there may be two sites at which Na+ activates Cl- secretion. Plots of 1/Isc vs. 1/[Cl-] with different [NA+] indicated, that the affinity of the Cl- "carrier" may be affected by [Na+]. stimulated tissues: Na+-free (choline replacement) solutions caused PD, Isc, and JClnet all to decrease to zero but sometimes Na+-containing mucosal solution caused JH to increase back to 50% of control, whereas Isc increased by only 16%. Na+-free effects were not reversed by 1 mM dibutyryl cAMP plus 0.1 mM isobutyl methylxanthine in the serosal solution. As [Na+] was increased, Isc (sigmoidal) and JH (monotonic) both increased. K+ replacement of Na+ caused a larger decrease in Isc than when choline was used; JH remained constant if [Na+] greater than or equal to mM. We have proposed that the energy-dependent step for active Cl- transport occurs at the serosal membrane in a Na+-coupled process. Cl- that accompanies JH during open-circuit conditions may utilize a separate system.

Analysis of amiloride inhibition of chorda tympani taste response of rat to NaCl

1985 ◽  
Vol 249 (1) ◽  
pp. R52-R61 ◽  
Author(s):  
J. A. DeSimone ◽  
F. Ferrell
Keyword(s):  
Time Course ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Chorda Tympani ◽  
Lingual Epithelium ◽  
Taste Response ◽  
Series Of Experiments ◽  
Kinetics Of ◽  
Kinetics Of Inhibition

The kinetics of inhibition by amiloride of the integrated chorda tympani response were investigated in rats subjected to lingual stimulation with NaCl. In one series of experiments the time of exposure to amiloride was varied at fixed amiloride concentration. Exposure to 10(-4) M amiloride for 2 s reduced the response to 0.5 M NaCl by approximately 50%. The time course of recovery from amiloride inhibition was first order (relaxation time approximately equal to 4 min) for all exposure times. For exposure to 10(-4) M amiloride for less than or equal to 30 s recovery was better than 90% in 20 min. Not all of the chorda tympani response was inhibited by amiloride. With 0.5 M NaCl there was a 70% reduction in response, whereas at 0.05 M NaCl the reduction was only 30%. Parallel effects of amiloride were seen in the short-circuit current of an in vitro preparation of canine lingual epithelium. Amiloride reduced the short-circuit current by the same percentage as it inhibited the chorda tympani response. These results suggest that gustatory transduction is mediated in part by an apical membrane transport system that can be inhibited by amiloride. There exists, however, a second transducing element that is amiloride insensitive. A model is developed, assuming, in part, that the neural response reflects the flows of Na through amiloride-sensitive apical pathways.

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