Site-specific regulation of ion transport by prolactin in rat colon epithelium

2012 ◽  
Vol 302 (10) ◽  
pp. G1199-G1206 ◽  
Author(s):  
Chatsri Deachapunya ◽  
Sutthasinee Poonyachoti ◽  
Nateetip Krishnamra

The effect of prolactin (PRL) on ion transport across the rat colon epithelium was investigated using Ussing chamber technique. PRL (1 μg/ml) induced a sustained decrease in short-circuit current ( Isc) in the distal colon with an EC50 value of 100 ng/ml and increased Isc in the proximal colon with an EC50 value of 49 ng/ml. In the distal colon, the PRL-induced decrease in Isc was not affected by Na+ channel blocker amiloride or Cl− channel blockers, NPPB, DPC, or DIDS, added mucosally. However, the response was inhibited by mucosal application of K+ channel blockers glibenclamide, quinidine, and chromanol 293B, whereas other K+ channel blockers, Ba2+, tetraethylammonium, clotrimazole, and apamin, failed to have effects. The PRL-induced decrease in Isc was also inhibited by Na+-K+-2Cl− transporter inhibitor bumetanide, Ba2+, and chromanol 293B applied serosally. In the transverse and proximal colon, the PRL-induced increase in Isc was suppressed by DPC, glibenclamide, and bumetanide, but not by NPPB, DIDS, or amiloride. The PRL-induced changes in Isc in both distal and proximal colon were abolished by JAK2 inhibitor AG490, but not BAPTA-AM, the Ca2+ chelating agent, or phosphatidylinositol 3-kinase inhibitor wortmannin. These results suggest a segment-specific effect of PRL in rat colon, by activation of K+ secretion in the distal colon and activation of Cl− secretion in the transverse and proximal colon. Both PRL actions are mediated by JAK-STAT-dependent pathway, but not phosphatidylinositol 3-kinase pathway or Ca2+ mobilization. These findings suggest a role of PRL in the regulation of electrolyte transport in mammalian colon.

1998 ◽  
Vol 275 (6) ◽  
pp. G1367-G1376 ◽  
Author(s):  
Silke Hörger ◽  
Gerhard Schultheiß ◽  
Martin Diener

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.


2000 ◽  
Vol 278 (2) ◽  
pp. C336-C343 ◽  
Author(s):  
W. Qiu ◽  
B. Lee ◽  
M. Lancaster ◽  
W. Xu ◽  
S. Leung ◽  
...  

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.


1985 ◽  
Vol 249 (1) ◽  
pp. G113-G119 ◽  
Author(s):  
J. H. Sellin ◽  
R. C. DeSoignie

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)


1998 ◽  
Vol 275 (5) ◽  
pp. G1166-G1172 ◽  
Author(s):  
Rainer Cermak ◽  
Ursula Föllmer ◽  
Siegfried Wolffram

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.


1995 ◽  
Vol 36 (2) ◽  
pp. 210-214 ◽  
Author(s):  
F. Pomerri ◽  
G. Gasparini ◽  
A. Martin ◽  
W. Fries ◽  
E. Pagiaro ◽  
...  

The colon of 32 healthy Sprague-Dawley rats was studied microradiographically. The colonic arterial distribution of 18 rats was examined after injecting barium sulfate into the isolated aorta. The mucosal surface in 9 rats was studied using double-contrast technique after colon explantation. In 5 animals arterial and mucosal studies were carried out simultaneously. The radiographic thickness of the colonic wall was measured using a comparative microscope. The specimens were observed, photographed and examined histologically. Unlike the cecum and distal colon which, when insufflated, do not have mucosal folds, the proximal colon exhibits folds in an oblique direction corresponding to that of the arteries, and the colonic wall in this region is thicker. Comparison between arterial and mucosal microradiographic anatomy and wall thickness enables the proposition of a simple nontopographic division of the rat colon into cecum, proximal colon and distal colon.


2013 ◽  
Vol 14 (7) ◽  
pp. 13577-13591 ◽  
Author(s):  
Wennan Zhao ◽  
Wenzhi Guo ◽  
Qianxiang Zhou ◽  
Sheng-Nan Ma ◽  
Ran Wang ◽  
...  

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