Effect of aldosterone and dexamethasone pretreatment on sodium transport in rat distal colon in vitro

1984 ◽  
Vol 400 (3) ◽  
pp. 257-261 ◽  
Author(s):  
R. D. Perrone ◽  
E. A. Alexander ◽  
H. H. Bengele ◽  
J. H. Schwartz
Keyword(s):  
Sodium Transport ◽  
Distal Colon ◽  
Rat Distal Colon

Bicarbonate secretion in rat distal colon in vitro: a measurement technique

1988 ◽  
Vol 254 (3) ◽  
pp. C383-C390 ◽  
Author(s):  
G. M. Feldman ◽  
S. F. Berman ◽  
R. L. Stephenson
Keyword(s):  
Short Circuit ◽  
Distal Colon ◽  
Apparent Permeability ◽  
Chemical Gradients ◽  
Acid Generation ◽  
Rat Distal Colon ◽  
Tissue Surfaces ◽  
Apparent Permeability Coefficient ◽  
Transepithelial Voltage

To study HCO3- secretion in rat distal colon, we utilized a technique that permits control of electrical and chemical transepithelial gradients. With symmetrical solutions (pH 7.4, [HCO3-] 25 mM, and CO2 tension 40 mmHg) bathing both tissue surfaces and under short-circuit conditions, HCO3- secretion remained stable for greater than 4 h at 1 mueq. h-1.cm-2. As the mucosal solution was alkalinized, the serosal solution was acidified at 3.1 mueq.h-1.cm-2. Ninety-four percent of serosal acidification was accounted for by the rate of metabolic lactic acid generation and transepithelial HCO3- secretion. Clamping transepithelial voltage reversibly affected net HCO3- secretion, and a linear relationship existed between clamped mucosal voltage and net HCO3- flux (r = 0.99); mucosal voltage of -68 mV completely inhibited net secretion. The apparent permeability coefficient of the colon to HCO3- is 2.8 X 10(-6) cm/s. One millimolar ouabain completely inhibited net HCO3- secretion. Acetazolamide (10(-4) M) inhibited secretion by approximately 50%, whereas a 10(-3) M concentration inhibited secretion by 90%. These data demonstrate that net colonic HCO3- secretion can be measured without imposed electrical and chemical gradients and that this flux is voltage sensitive and depends on carbonic anhydrase and Na+-K+-ATPase activities.

Functional studies of in vitro rat distal colon before and after restitution

Surgery ◽  
1997 ◽  
Vol 121 (4) ◽  
pp. 430-439 ◽  
Author(s):  
Madhu Prasad ◽  
Susumu Ito ◽  
William Silen
Keyword(s):  
Distal Colon ◽  
Functional Studies ◽  
Rat Distal Colon ◽  
Before And After

scholarly journals Aldosterone induces active K+ secretion by enhancing mucosal expression of Kcnn4c and Kcnma1 channels in rat distal colon

2012 ◽  
Vol 302 (9) ◽  
pp. C1353-C1360 ◽  
Author(s):  
Satish K. Singh ◽  
Bryan O'Hara ◽  
Jamilur R. Talukder ◽  
Vazhaikkurichi M. Rajendran
Keyword(s):  
Channel Blocker ◽  
Short Circuit ◽  
Distal Colon ◽  
Normal Colonic Mucosa ◽  
Transcriptional Level ◽  
Mrna Levels ◽  
Atpase Inhibitor ◽  
Synthesis Inhibitor ◽  
Rat Distal Colon

Although both Kcnn4c and Kcnma1 channels are present on colonic mucosal membranes, only Kcnma1 has been suggested to mediate K+ secretion in the colon. Therefore, studies were initiated to investigate the relative roles of Kcnn4c and Kcnma1 in mediating aldosterone (Na-free diet)-induced K+ secretion. Mucosal to serosal (m-s), serosal to mucosal (s-m), and net 86Rb+ (K+ surrogate) fluxes as well as short circuit currents ( Isc; measure of net ion movement) were measured under voltage clamp condition in rat distal colon. Active K+ absorption, but not K+ secretion, is present in normal, while aldosterone induces active K+ secretion (1.04 ± 0.26 vs. −1.21 ± 0.15 μeq·h−1·cm−2; P < 0.001) in rat distal colon. Mucosal VO4 (a P-type ATPase inhibitor) inhibited the net K+ absorption in normal, while it significantly enhanced net K+ secretion in aldosterone animals. The aldosterone-induced K+ secretion was inhibited by the mucosal addition of 1) either Ba2+ (a nonspecific K+ channel blocker) or charybdotoxin (CTX; a common Kcnn4 and Kcnma1 channel blocker) by 89%; 2) tetraethyl ammonium (TEA) or iberiotoxin (IbTX; a Kcnma1 channel blocker) by 64%; and 3) TRAM-34 (a Kcnn4 channel blocker) by 29%. TRAM-34, but not TEA, in the presence of IbTX further significantly inhibited the aldosterone-induced K+ secretion. Thus the aldosterone-induced Ba2+/CTX-sensitive K+ secretion consists of IbTX/TEA-sensitive (Kcnma1) and IbTX/TEA-insensitive fractions. TRAM-34 inhibition of the IbTX-insensitive fraction is consistent with the aldosterone-induced K+ secretion being mediated partially via Kcnn4c. Western and quantitative PCR analyses indicated that aldosterone enhanced both Kcnn4c and Kcnma1α protein expression and mRNA abundance. In vitro exposure of isolated normal colonic mucosa to aldosterone also enhanced Kcnn4c and Kcnma1α mRNA levels, and this was prevented by exposure to actinomycin D (an RNA synthesis inhibitor). These observations indicate that aldosterone induces active K+ secretion by enhancing mucosal Kcnn4c and Kcnma1 expression at the transcriptional level.

Aldosterone and PCO2 enhance rubidium absorption in rat distal colon

1988 ◽  
Vol 254 (6) ◽  
pp. G898-G906 ◽  
Author(s):  
R. D. Perrone ◽  
D. E. McBride
Keyword(s):  
Partial Pressure ◽  
Proton Pump ◽  
Distal Colon ◽  
Rat Colon ◽  
Rabbit Colon ◽  
Partial Pressure Of Co2 ◽  
Rat Distal Colon

Recent studies of rabbit colon have indicated the presence of a vanadate-sensitive K+-dependent proton pump, suggesting the existence of an H+-K+-ATPase. The participation of such a mechanism for colonic K+ absorption in the rat has not been determined. To this purpose, we attempted to detect the presence of pH-linked mechanisms for K+ absorption in rat distal colon using 86Rb as a marker for K+. We found that Rb+ absorption in Na-Ringer directly correlated with the in vitro partial pressure of CO2 (PCO2) in aldosterone-stimulated but not in control rats. Similar studies performed using Na-free Ringer demonstrated that PCO2 markedly augmented Rb+ absorption in both control and aldosterone-stimulated rat colon. Rb+ absorption was inhibited by orthovanadate, SCH28080, and mucosal ouabain in Na-free Ringer, but there was no effect of omeprazole, furosemide, or bumetanide. Barium applied to the serosa was also effective in inhibiting Rb+ absorption, suggesting that Rb+ exit from the cell was conductive. These findings are consistent with the presence of an active K+ pump that is activated by pretreatment with aldosterone and increased in vitro PCO2 and that is inhibited by orthovanadate, SCH28080, and mucosal ouabain. The constellation of findings suggests that participation of an ATPase that is not typical of either Na+-K+-ATPase or H+-K+-ATPase.

Sign in / Sign up

Export Citation Format

Share Document