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.

scholarly journals Segment-specific effects of epinephrine on ion transport in the colon of the rat

1998 ◽  
Vol 275 (6) ◽  
pp. G1367-G1376 ◽  
Author(s):  
Silke Hörger ◽  
Gerhard Schultheiß ◽  
Martin Diener
Keyword(s):  
Ion Transport ◽  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Proximal Colon ◽  
Rat Colon ◽  
Second Phase ◽  
Stimulatory Action ◽  
Β Receptor

The effect of epinephrine on transport of K+, Na+, Cl−, and[Formula: see text] across the rat colon was studied using the Ussing chamber technique. Epinephrine (5 × 10−6mol/l) induced a biphasic change in short-circuit current ( Isc) in distal and proximal colon: a transient increase followed by a long-lasting decay. The first phase of the Iscresponse was abolished in Cl−-poor solution or after bumetanide administration, indicating a transient induction of Cl−secretion. The second phase of the response to epinephrine was suppressed by apical administration of the K+channel blocker, quinine, and was concomitant with an increase in serosal-to-mucosal Rb+flux, indicating that epinephrine induced K+secretion, although this response was much smaller than the change in Isc. In addition, the distal colon displayed a decrease in mucosal-to-serosal and serosal-to-mucosal Cl−fluxes when treated with epinephrine. In the distal colon, indomethacin abolished the first phase of the epinephrine effect, whereas the second phase was suppressed by TTX. In the proximal colon, indomethacin and TTX were ineffective. The neuronally mediated response to epinephrine in the distal colon was suppressed by the nonselective β-receptor blocker, propranolol, and by the β2-selective blocker, ICI-118551, whereas the epithelial response in the proximal colon was suppressed by the nonselective α-blocker, phentolamine, and by the selective α2-blocker, yohimbine. These results indicate a segment-specific action of epinephrine on ion transport: a direct stimulatory action on epithelial α2-receptors in the proximal colon and an indirect action on secretomotoneurons via β2-receptors in the distal colon.

Control of electrogenic Na+ absorption in rat late distal colon by nanomolar aldosterone added in vitro

1993 ◽  
Vol 264 (1) ◽  
pp. E68-E73 ◽  
Author(s):  
M. Fromm ◽  
J. D. Schulzke ◽  
U. Hegel
Keyword(s):  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Proximal Colon ◽  
Hill Coefficient ◽  
Late Response ◽  
Maximal Velocity ◽  
Time Courses

It has been possible to obtain in a mammalian epithelium of dietetically and surgically untreated animals a dose response of in vitro-added aldosterone (Aldo, 10(-10) to 10(-5) M) on electrogenic Na+ absorption (JeNa). JeNa was measured in the Ussing chamber on stripped rat late distal colon 8 h after in vitro addition of Aldo. Submaximal effects were obtained at 3 nM Aldo; after a lag time of 2 h, short-circuit current (Isc) increased to a maximum of 234 +/- 15 microA/cm2 and dropped after 0.1 mM amiloride to -18 +/- 3 microA/cm2, resulting in JeNa of 9.4 +/- 0.6 mumol.h-1 x cm-1. Net Na+ tracer fluxes and Isc exhibited parallel time courses, so that electroneutral Na+ transport was not induced in late distal colon by acute Aldo. A plot of JeNa vs. Na conductance revealed an electromotive force (ENa) of 126 +/- 1 mV for all Aldo concentrations tested. Kinetic data were as follows: Michaelis constant 1.2 nM, maximal velocity (Vmax) 10.5 mumol.h-1 x cm-2, and Hill coefficient 2.1. In contrast to the large effect in late distal colon, 3 nM Aldo caused JeNa of < 1 mumol.h-1 x cm-2 in early distal colon, proximal colon, and cecum. Antimineralocorticoid sensitivity and ENa did not vary with Aldo concentration or time of the experiment, consistent with a unique mechanism during the early and late response up to 8 h, as well as at mineralocorticoid and glucocorticoid Aldo concentrations. Acute Aldo in a range of 0.1–10 nM fully controls JeNa between zero and Vmax in late distal colon.(ABSTRACT TRUNCATED AT 250 WORDS)

Antisecretory effect of prostaglandin D2 in rat colon in vitro: action sites

1991 ◽  
Vol 260 (6) ◽  
pp. G904-G910 ◽  
Author(s):  
K. J. Goerg ◽  
C. Diener ◽  
M. Diener ◽  
W. Rummel
Keyword(s):  
Short Circuit ◽  
Ussing Chamber ◽  
Short Circuit Current ◽  
Rat Colon ◽  
Prostaglandin D2 ◽  
Cyclic Monophosphate ◽  
Heat Stable ◽  
Antisecretory Effect ◽  
Flux Measurements

The effect of prostaglandin D2 (PGD2) on colonic ion transport was studied in the Ussing chamber. PGD2 (10(-6) M) decreased baseline short-circuit current (Isc) in two preparations of rat colon descendens, a mucosa-submucosa preparation with and a mucosa preparation without the submucosal plexus. In both preparations, PGD2 inhibited the neuronally mediated secretory responses to electric field stimulation, the sea anemone toxin ATX II, and different cholinergic agents. Unidirectional flux measurements revealed that PGD2 diminished the secretagogue-induced increase in the serosal-to-mucosal flux of Cl- and thereby inhibited net Cl- secretion. PGD2, however, had no effect on the adenosine 3',5'-cyclic monophosphate-mediated response to forskolin or vasoactive intestinal peptide or on guanosine 3',5'-cyclic monophosphate-mediated secretion induced by the heat-stable enterotoxin of Escherichia coli. The PGD2 also blocked the increase in Isc evoked by two neuronally acting inflammatory mediators, i.e., bradykinin and PGI2 in the mucosa-submucosa preparation, but had no effect on the response to PGE2. Consequently, PGD2 exerts an indirect antisecretory effect caused by an inhibition of enteric secretomotor neurons of both the submucosal and the mucosal plexus.

Galanin-induced alteration of electrolyte transport in the rat intestine

1992 ◽  
Vol 263 (4) ◽  
pp. G502-G507
Author(s):  
T. Kiyohara ◽  
M. Okuno ◽  
H. Ishikawa ◽  
T. Nakanishi ◽  
Y. Shinomura ◽  
...  
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Electrical Field Stimulation ◽  
Distal Colon ◽  
Rat Colon ◽  
Chloride Absorption ◽  
Neural Transmission ◽  
36Cl Fluxes ◽  
Intestinal Ion Transport

Effects of rat and porcine galanin on rat intestinal ion transport were examined in vitro. In the rat distal colon, a sustained increase in short-circuit current (Isc) was produced by the serosal addition of rat galanin at a concentration as low as 10(-9) M, and a maximal increment was observed at 10(-7) M. Porcine galanin was approximately 100 times less potent than rat galanin. In the rat jejunum, rat galanin produced only a slight and transient decrease in basal Isc. The response to rat galanin was not influenced by atropine, hexamethonium, or amiloride, but was virtually abolished by tetrodotoxin or furosemide. Rat galanin did not significantly influence the increase in Isc elicited by electrical field stimulation in the rat colon and jejunum. Transmural unidirectional 22Na and 36Cl fluxes in the rat colonic mucosa were measured under short-circuited conditions, and rat galanin significantly decreased net sodium and net chloride absorption. These findings suggest that galanin acts as a secretory modulator in the rat colon via noncholinergic neural transmission.

Cyclic nucleotide-gated cation channels mediate sodium and calcium influx in rat colon

2000 ◽  
Vol 278 (2) ◽  
pp. C336-C343 ◽  
Author(s):  
W. Qiu ◽  
B. Lee ◽  
M. Lancaster ◽  
W. Xu ◽  
S. Leung ◽  
...  
Keyword(s):  
Cyclic Nucleotide ◽  
Calcium Absorption ◽  
Calcium Influx ◽  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Proximal Colon ◽  
Cation Channels ◽  
Rat Colon ◽  
Sodium Absorption

We found mRNA for the three isoforms of the cyclic nucleotide-gated nonselective cation channel expressed in the mucosal layer of the rat intestine from the duodenum to the colon and in intestinal epithelial cell lines in culture. Because these channels are permeable to sodium and calcium and are stimulated by cGMP or cAMP, we measured 8-bromo-cGMP-stimulated sodium-mediated short-circuit current ( I sc) in proximal and distal colon and unidirectional45Ca2+fluxes in proximal colon to determine whether these channels could mediate transepithelial sodium and calcium absorption across the colon. Sodium-mediated I sc, stimulated by 8-bromo-cGMP, were inhibited by dichlorobenzamil and l-cis-diltiazem, blockers of cyclic nucleotide-gated cation channels, suggesting that these ion channels can mediate transepithelial sodium absorption. Sodium-mediated I sc and net transepithelial45Ca2+absorption were stimulated by heat-stable toxin from Escherichia coli that increases cGMP. Addition of l-cis-diltiazem inhibited the enhanced transepithelial absorption of both ions. These results suggest that cyclic nucleotide-gated cation channels simultaneously increase net sodium and calcium absorption in the colon of the rat.

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)

Suppression of coupled Na-Cl absorption by aldosterone and dexamethasone in rat distal colon in vitro

1984 ◽  
Vol 246 (6) ◽  
pp. F785-F793 ◽  
Author(s):  
R. D. Perrone ◽  
S. L. Jenks
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Rat Colon ◽  
Na Transport ◽  
Unidirectional Flux ◽  
Rat Distal Colon ◽  
Marked Suppression ◽  
Stimulation Of

Basal Na absorption in the rat colon is coupled to that of Cl in an electroneutral fashion. We previously determined that aldosterone or dexamethasone induces amiloride-sensitive mucosal-to-serosal Na flux approximately equal to the amiloride-sensitive short-circuit current in rat distal colon in vitro. However, the effect of these steroids on coupled Na-Cl absorption was not examined. For this purpose, we determined the unidirectional flux of Na and Cl in voltage-clamped distal colon segments from rats treated with aldosterone or dexamethasone. Amiloride was used as a probe for conductive Na absorption, and acetazolamide and Cl-free solutions were used as probes for coupled Na-Cl absorption. Our results indicate that the nature of colonic Na absorption is markedly changed after treatment with these steroids. In contrast to findings in the untreated rat, colonic Na absorption after treatment with aldosterone or dexamethasone was largely independent of the presence of Cl. Net Cl absorption and acetazolamide sensitivity were both greatly diminished. Thus, aldosterone and dexamethasone have multiple effects on Na transport in rat distal colon. In addition to the stimulation of conductive Na absorption by aldosterone, an effect well described in other epithelia, there is marked suppression of coupled Na-Cl absorption. Dexamethasone was less effective in suppressing Cl absorption but equally effective in stimulating conductive Na absorption. These steroid effects were greater in the terminal 1-2 cm of the rat colon.

Low-dose glucocorticoids maintain Na-H exchange in distal colon of adrenalectomized rats

1991 ◽  
Vol 261 (3) ◽  
pp. F545-F553 ◽  
Author(s):  
C. P. Bastl ◽  
L. Bressler ◽  
G. Schulman ◽  
M. Mendez ◽  
E. J. Cragoe
Keyword(s):  
Short Circuit ◽  
In Vitro Study ◽  
Short Circuit Current ◽  
Distal Colon ◽  
Ion Flux ◽  
Rat Colon ◽  
Anion Secretion ◽  
Stimulation Of

With in vivo perfusion we demonstrated that physiological doses of glucocorticoids restore Na and Cl absorption in adrenalectomized rat colon. The absorption is spironolactone and amiloride resistant and is inhibited by the Na-H inhibitor, 5-(N-ethyl-N-isopropyl)amiloride (EIPA), suggesting that glucocorticoids modulate Na-H antiport. The present in vitro study examines pathways mediated by glucocorticoids in adrenalectomized rat distal colon and rectum. In vivo administration of 2.5 micrograms/100 g body wt dexamethasone did not alter serosal-to-mucosal flux or tissue electrical parameters but restored mucosal-to-serosal flux and net Na and Cl absorption within 2–3 h of administration to levels found in intact rat colon. Transport was not inhibited by 10(-5) M amiloride but was eliminated by 10(-5) M EIPA. After 26 h of dexamethasone, an amiloride-resistant short-circuit current was stimulated, accompanied by increased residual ion flux in rectum, but not distal colon, suggesting that a delayed or secondary effect of glucocorticoids is stimulation of electrogenic anion secretion. Thus adrenalectomy reduces net ion flux in distal colon by its effect on electroneutral mucosal-to-serosal NaCl flux. Small doses of glucocorticoids completely ameliorate this effect via stimulation of the Na-H antiport. Glucocorticoids maintain basal electroneutral NaCl absorption in distal rat colon.

Role of calcium in the regulation of colonic secretion in the rat

1983 ◽  
Vol 244 (5) ◽  
pp. G552-G560 ◽  
Author(s):  
T. W. Zimmerman ◽  
J. W. Dobbins ◽  
H. J. Binder
Keyword(s):  
Short Circuit ◽  
Short Circuit Current ◽  
Chloride Secretion ◽  
Extracellular Calcium ◽  
Electrolyte Transport ◽  
Rat Colon ◽  
Sodium Absorption ◽  
Chloride Absorption

In vitro experiments were performed in rat colon to define the role of calcium in the regulation of electrolyte transport. Neither basal net sodium absorption (JNanet) nor JClnet was affected by varying serosal calcium from 0 to 3.0 mM, but both were decreased by 4.8 mM calcium. Removal of serosal calcium completely inhibited the effect of bethanechol, a muscarinic cholinergic agonist, which inhibits neutral sodium-chloride absorption in 1.2 mM calcium. In contrast, theophylline significantly decreased JNanet and JClnet both in the presence and absence of calcium, but the effects of theophylline were significantly less in calcium-free media. In 3.0 mM calcium bethanechol inhibited JCLnet significantly greater than JNanet and in 4.8 mM calcium bethanechol decreased JClnet equivalent to the increase in short-circuit current without significantly altering JNanet. We conclude that 1) high [Ca2+] inhibits net sodium and net chloride absorption; 2) the alteration of electrolyte transport by bethanechol is dependent on extracellular calcium, and the alteration of electrolyte transport by theophylline is not dependent on extracellular calcium but may be dependent on intracellular calcium; and 3) in addition to inhibition of neutral NaCl absorption, bethanechol stimulates chloride secretion.

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.

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