Dietary potassium modulates active potassium absorption and secretion in rat distal colon

1986 ◽  
Vol 251 (5) ◽  
pp. G619-G626 ◽  
Author(s):  
E. S. Foster ◽  
G. I. Sandle ◽  
J. P. Hayslett ◽  
H. J. Binder

To determine the effect of variations in body stores of potassium on the rate of active potassium transport in the large intestine, unidirectional 42K fluxes were performed under short-circuit conditions across isolated distal colonic mucosa of control, dietary potassium-depleted and dietary potassium-loaded rats. Potassium depletion stimulated net potassium absorption (JK net) (0.87 +/- 0.19 vs. 0.49 +/- 0.04 mu eq X h-1 X cm-2, P less than 0.025) due to a 40% increase in mucosal-to-serosal potassium transport (JK m----s). In sodium-free Ringer solution JK net in the potassium-depleted group was also significantly greater than in controls (1.93 +/- 0.26 vs. 1.01 +/- 0.11 mu eq X h-1 X cm-2, P less than 0.005). In contrast, in chloride-free Ringer solution JK net was identical in the control and potassium-depleted groups (0.39 +/- 0.05 vs. 0.46 +/- 0.07 mu eq X h-1 X cm-2, P = NS). Potassium loading reversed net potassium absorption to net potassium secretion (-0.76 +/- 0.08 mu eq X h-1 X cm-2, P less than 0.001) as the result of a decrease in JK m----s and an increase in serosal-to-mucosal potassium transport (JK s----m). Net potassium secretion was abolished in the absence of either sodium or chloride from the bathing solution but not by mucosal amiloride. In sodium-free Ringer solution JK net was similar in control and potassium-loaded groups, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

1983 ◽  
Vol 245 (5) ◽  
pp. G668-G675 ◽  
Author(s):  
E. S. Foster ◽  
T. W. Zimmerman ◽  
J. P. Hayslett ◽  
H. J. Binder

To determine the effect of corticosteroids on active transport processes, unidirectional fluxes of 22Na, 36Cl, and 42K were measured under short-circuit conditions across isolated stripped distal colonic mucosa of the rat in control, secondary hyperaldosterone, and dexamethasone-treated animals. In controls net sodium and chloride fluxes (JNanet and JClnet) and short-circuit current (Isc) were 6.6 +/- 2.2, 7.6 +/- 1.6, and 1.3 +/- 0.2 mu eq X h-1 X cm-2, respectively. Although aldosterone increased Isc to 7.3 +/- 0.5 mu eq X h-1 X cm-2, JNanet (6.9 +/- 0.7 mu eq X h-1 X cm-2) was not altered and JClnet was reduced to 0 compared with controls. Dexamethasone also stimulated Isc but did not inhibit JClnet. In Cl-free Ringer both aldosterone and dexamethasone produced significant and equal increases in JNanet and Isc. Theophylline abolished JNanet in control animals but not in the aldosterone group. Aldosterone reversed net potassium absorption (0.58 +/- 0.11 mu eq X h-1 X cm-2) to net potassium secretion (-0.94 +/- 0.08 mu eq X h-1 X cm-2). Dexamethasone reduced net potassium movement to 0 (-0.04 +/- 0.12 mu eq X h-1 X cm-2). These studies demonstrate that 1) corticosteroids stimulate electrogenic sodium absorption and 2) aldosterone, but not dexamethasone, inhibits neutral NaCl absorption and stimulates active potassium secretion. The effects of mineralocorticoids and glucocorticoids on electrolyte transport are not identical and may be mediated by separate and distinct mechanisms.


1986 ◽  
Vol 251 (2) ◽  
pp. G249-G252 ◽  
Author(s):  
M. E. Budinger ◽  
E. S. Foster ◽  
J. P. Hayslett ◽  
H. J. Binder

Increased dietary potassium ("potassium loading") induces several adaptive changes in colonic function, including increased potential-dependent potassium secretion, active potassium secretion, and Na-K-ATPase activity, but does not alter net sodium absorption in vivo. To establish whether potassium loading stimulates active sodium transport, unidirectional, net sodium, and chloride fluxes were determined under voltage-clamp conditions across isolated rat distal colonic mucosa. In normal animals net sodium flux (JNanet), net chloride flux (JClnet) and short-circuit current (Isc) were 6.1 +/- 1.1, 8.4 +/- 1.0, and 0.7 +/- 0.1 mu eq X h-1. cm-2, respectively; potassium loading significantly increased JNanet and Isc by 4.9 +/- 1.4 and 3.5 +/- 0.7 mu eq X h-1 X cm-2, respectively, without changing JClnet. Amiloride (0.1 mM) inhibited the increases in JNanet and Isc produced by potassium loading. In Cl-free Ringer solution in normal animals JNanet was reduced to 0.6 +/- 0.3 mu eq X h-1 X cm-2. Potassium loading produced identical increases in JNanet and Isc, which were also completely inhibited by 0.1 mM amiloride. These studies establish that potassium loading induces amiloride-sensitive electrogenic sodium absorption without affecting electroneutral sodium-chloride absorption.


Gut ◽  
1999 ◽  
Vol 44 (1) ◽  
pp. 40-46 ◽  
Author(s):  
G I Sandle ◽  
I Butterfield

BackgroundChronic dietary K+ loading increases the abundance of large conductance (210 pS) apical K+ channels in surface cells of rat distal colon, resulting in enhanced K+ secretion in this epithelium. However, the factors involved in the regulation of these K+ channels are at present unclear.AimsTo evaluate the effect of dietary K+ loading on intracellular pH and its relation to large conductance apical K+ channel activity in surface cells of rat distal colon.Methods/ResultsAs assessed by fluorescent imaging, intracellular pH was higher in K+ loaded animals (7.48 (0.09)) than in controls (7.07 (0.04); p<0.01) when surface cells were bathed in NaCl solution, and a similar difference in intracellular pH was observed when cells were bathed in Na2SO4 solution (7.67 (0.09) and 6.92 (0.05) respectively; p<0.001). Ethylisopropylamiloride (EIPA; an inhibitor of Na+-H+ exchange; 1 μM) decreased intracellular pH when surface cells from K+ loaded animals were bathed in either solution, although the decrease was greater when the solution contained NaCl (ΔpH 0.50 (0.03)) rather than Na2SO4 (ΔpH 0.18 (0.02); p<0.05). In contrast, EIPA had no effect in cells from control animals. As assessed by patch clamp recording techniques, the activity of large conductance K+ channels in excised inside-out membrane patches from distal colonic surface cells of K+ loaded animals increased twofold when the bath pH was raised from 7.40 to 7.60. As assessed by cell attached patches in distal colonic surface cells from K+ loaded animals, the addition of 1 μM EIPA decreased K+ channel activity by 50%, consistent with reversal of Na+-H+ exchange mediated intracellular alkalinisation.ConclusionIntracellular alkalinisation stimulates pH sensitive large conductance apical K+ channels in rat distal colonic surface cells as part of the K+ secretory response to chronic dietary K+loading. Intracellular alkalinisation seems to reflect an increase in EIPA sensitive Na+-H+ exchange, which may be a manifestation of the secondary hyperaldosteronism associated with this model of colonic K+ adaptation.


1985 ◽  
Vol 403 (4) ◽  
pp. 433-439 ◽  
Author(s):  
G. I. Sandle ◽  
E. S. Foster ◽  
S. A. Lewis ◽  
H. J. Binder ◽  
J. P. Hayslett

1982 ◽  
Vol 242 (1) ◽  
pp. C81-C86 ◽  
Author(s):  
R. McCabe ◽  
H. J. Cooke ◽  
L. P. Sullivan

Unidirectional mucosal-to-serosal (Jm leads to s) and serosal-to-mucosal (Js leads to m) fluxes of potassium and sodium were determined simultaneously on paired sections of descending colon from the same rabbit under short-circuit conditions. In 13-16 pairs of tissues, net potassium secretion and sodium absorption averaged 0.49 +/- 0.08 and 4.0 +/- 0.8 mueq.cm-2.h-1, respectively. Short-circuit current (Jsc) averaged 3.7 +/- 0.4 mueq.cm-2.h-1 and was approximately equal to the algebraic sum of net potassium and sodium fluxes. Treatment of both sides of the colon with 10(-4) M ouabain reduced the Jsc and transmural potential difference to near zero. Ouabain abolished net potassium secretion by reducing JKs leads to m and abolished net sodium absorption by inhibiting JNam leads to s. In the presence of ouabain, net potassium absorption averaging 0.15 +/- 0.07 mueq.cm-2.h-1 (n = 11) was observed. In the presence of 10(-3) M 2,4-dinitrophenol, both net potassium and net sodium fluxes were abolished, primarily as a result of a reduction in JKs leads to m and JNam leads to s without altering JKm leads to s and JNas leads to m. These results suggest that the rabbit descending colon has the capacity to secrete and possibly to absorb potassium by active mechanisms requiring metabolic energy. Comparison of potassium and sodium fluxes suggest that the paracellular pathway in the rabbit colon is not potassium selective.


1984 ◽  
Vol 246 (5) ◽  
pp. G611-G617 ◽  
Author(s):  
E. S. Foster ◽  
J. P. Hayslett ◽  
H. J. Binder

To characterize and contrast the active potassium absorptive and secretory processes present in the rat colon, unidirectional 42K fluxes were performed under short-circuit conditions across isolated distal (D) and proximal (P) colonic mucosa of control rats and animals with hyperaldosteronism due to sodium depletion (aldosterone group). In the control D colon there was net potassium absorption (+0.51 +/- 0.07 mueq X h-1 X cm-2). The absorptive process appears electroneutral because net potassium flux ( JK net ) was unchanged in sodium-free Ringer solution (+0.76 +/- 0.12 mueq X h-1 X cm-2), whereas short-circuit current (Isc) was reduced to zero, and in chloride-free Ringer solution. In P colon of controls, net potassium secretion was -0.19 +/- 0.02 mueq X h-1 X cm-2 and was abolished by removal of sodium but not by removal of chloride. In both P and D colon aldosterone produced active potassium secretion (-0.39 +/- 0.06 mueq X h-1 X cm-2, P less than 0.001, and -0.90 +/- 0.07 mueq X h-1 X cm-2, P less than 0.001, respectively) that was sodium and chloride dependent. Although mucosal amiloride in D colon of aldosterone animals reduced net sodium flux to zero and reversed Isc from 4.1 +/- 0.6 to -1.1 +/- 0.1 mueq X h-1 X cm-2, net potassium secretion was not affected. Thus, in the presence of amiloride, Isc is accounted for by JK net (-0.93 +/- 0.12 mueq X h-1 X cm-2). These data indicate that 1) the active potassium absorptive process is electroneutral and could be explained by a potassium-proton exchange, and 2) the potassium secretory process is stimulated by aldosterone, is not inhibited by amiloride, and probably is electrogenic.


1979 ◽  
Vol 78 (1) ◽  
pp. 213-223
Author(s):  
DAVID F. MOFFETT

Potassium transport by the isolated midgut of Manduca larvae, as measured by the short circuit current, is inhibited by substitution of small organic solutes (M.W. &lt; 340) for the sucrose normally included in bathing solution formulated for this tissue. Other solutes of molecular weight equal to or greater than sucrose are essentially as effective as sucrose in promoting the short circuit current. Equilibration of midgut in solutions containing the small solute mannitol results in a decrease in the dry weight/wet weight ratio of the tissue, suggesting that the small solutes can penetrate into areas of the tissue which are not accessible to sucrose. Histological studies suggest that sites of swelling in the presence of mannitol include both cytoplasm and goblet cell lumen. The inhibition of the short circuit current is rapidly reversible on return to bathing solution containing sucrose or another large solute. The effect of small solutes probably does not involve compromise of the energy source for potassium transport since oxygen uptake is unchanged in the presence of a small solute.


1988 ◽  
Vol 254 (3) ◽  
pp. C383-C390 ◽  
Author(s):  
G. M. Feldman ◽  
S. F. Berman ◽  
R. L. Stephenson

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.


1986 ◽  
Vol 251 (2) ◽  
pp. F199-F207
Author(s):  
S. K. Mujais ◽  
M. A. Chekal ◽  
J. P. Hayslett ◽  
A. I. Katz

The purpose of this study was to characterize the alterations in collecting tubule Na+-K+-ATPase activity produced by sustained increments in dietary potassium in the rat and to evaluate the role of aldosterone in their generation. In adrenal-intact animals, feeding a high-potassium diet (10-fold that of control) or administration of a high physiological dose of aldosterone (5 micrograms X 100 g-1 X day-1), which simulates the delivery rate of this hormone during potassium loading (both for 7 days), caused marked increments in Na+-K+-ATPase activity in the cortical collecting tubule (CCT) but had no effect on the enzyme in the inner stripe of the medullary collecting tubule (MCT). A significant increase in enzyme activity was also observed after smaller dietary potassium increments (2.5 and 5 times the control) and after 4 (but not 2) days of dietary potassium load. In adrenalectomized rats provided with physiological replacement doses of corticosterone and aldosterone (0.8 micrograms X 100 g-1 X day-1), Na+-K+-ATPase activity in both CCT and MCT was similar to that of adrenal-intact controls but remained unchanged after 7 days on the potassium-enriched (10-fold) diet. In contrast, adrenalectomized animals receiving the high physiological dose of aldosterone displayed an increase in Na+-K+-ATPase activity of CCT comparable with that of adrenal-intact animals, whereas the enzyme activity in the MCT was unaffected. In conclusion, 1) following chronic potassium loading Na+-K+-ATPase activity increases significantly in the CCT with no change in its activity in the inner stripe of the MCT.(ABSTRACT TRUNCATED AT 250 WORDS)


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