Ion Transport in Rat Colon

Author(s):  
Vazhaikkurichi M. Rajendran ◽  
Henry J. Binder
Keyword(s):  
1997 ◽  
Vol 54 (10) ◽  
pp. 1133-1137 ◽  
Author(s):  
Declan F McCole ◽  
Barbara Otti ◽  
Philip Newsholme ◽  
Alan W Baird

Digestion ◽  
2001 ◽  
Vol 63 (2) ◽  
pp. 124-129 ◽  
Author(s):  
Maeve M. Skelly ◽  
Diarmuid P. O’Donoghue ◽  
Alan W. Baird

2001 ◽  
Vol 415 (2-3) ◽  
pp. 277-283 ◽  
Author(s):  
Riccardo Patacchini ◽  
Helen M Cox ◽  
Sandra Ståhl ◽  
Iain R Tough ◽  
Carlo Alberto Maggi

1988 ◽  
Vol 81 (6) ◽  
pp. 1903-1910 ◽  
Author(s):  
D S Goldfarb ◽  
R W Egnor ◽  
A N Charney
Keyword(s):  

1982 ◽  
Vol 242 (2) ◽  
pp. G116-G123 ◽  
Author(s):  
T. W. Zimmerman ◽  
J. W. Dobbins ◽  
H. J. Binder

Cholinergic agonists inhibit sodium and chloride absorption in the intestine and often produce secretion. To determine the mechanism of cholinergic regulation of intestinal electrolyte transport, the effects of bethanechol on ion transport were studied in the rat colon in vitro. The addition of 1 mM bethanechol produced an initially large but short-lived increase in short-circuit current (Isc) (171 +/- 19 microA/cm2). Bethanechol decreased net sodium and net chloride absorption (2.5 +/- 0.5 and 2.9 +/- 0.9 mueq . h-1 . cm-2, respectively) and increased Isc (0.8 +/- 0.3 mueq . h-1 . cm-2) during the steady-state period. All these effects were inhibited by 1 microM atropine, which alone had no effect on ion transport. The removal of either sodium or chloride also inhibited the effect of bethanechol. cAMP content did not increase in isolated enterocytes incubated with bethanechol; however, calcium removal from the serosal bathing solution inhibited the bethanechol-induced changes in ion transport. These results indicate that cholinergic muscarinic agonists alter sodium and chloride transport in the colon by inhibiting coupled NaCl absorption by a calcium-dependent, non-cAMP-mediated process.


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.


1977 ◽  
Vol 272 (3) ◽  
pp. 737-754 ◽  
Author(s):  
J. G. Browning ◽  
Jacqueline Hardcastle ◽  
P. T. Hardcastle ◽  
P. A. Sanford
Keyword(s):  

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