K+ transport by rat colon: adaptation to a low potassium diet

Abstract

Recent studies with the isolated perfused rat kidney have demonstrated the existence of an intrinsic renal adaptation to conserve K+ in response to ingestion of a low K+ diet for 3 days. To determine whether the colon alters its K+ transport properties in a similar fashion, we measured transmural 86Rb fluxes across sheets of distal colonic epithelium under short-circuit conditions. Preliminary studies using a double-isotope technique demonstrated that 86Rb and 42K fluxes were similar; therefore 86Rb flux was considered equivalent to K+ flux. The distal half of the colon from each rat was divided into two segments, referred to as early and late distal colon. Experiments were carried out using rats fed a K+ -free, control (0.15 mmol/g), and high K+ (1.13 mmol/g) powdered diet of otherwise identical electrolyte content. Net K+ secretion (Jnet) by the early distal colon was reduced from 0.45 in the controls to -0.02 mueq X cm-2 X h-1 by a low K+ diet as a result of a decrease in serosal-to-mucosal flux (Jsm), with no change in mucosal-to-serosal flux (Jms). Conductance (GT) and short-circuit current (Isc) were unchanged. Jnet by the late distal colon averaged 0.17 in the controls and 0.01 mueq X cm-2 X h-1 with a low K+ diet, but this difference was not significant statistically. In comparison with the controls, a high K+ diet had no effect on Jnet by the early distal colon (0.48 mueq X cm-2 X h-1) but increased Jnet by the late distal colon substantially (0.77 mueq X cm-2 X h-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone stimulates K secretion across mammalian colon independent of Na absorption.

“…(iii) JKt after inhibition of the negative ISc was not significantly different in control and aldosterone-treated tissues, suggesting that the active absorptive capacity for K was unchanged by aldosterone addition. Previous studies of K transport from chronically treated animals also indicated that active K absorption was not altered by elevated plasma aldosterone (15,16). These three results support the model for K transport shown in Fig.…”

Cellular site of active K absorption in the guinea-pig distal colonic epithelium

“…Taking into account that the mucosal surface is not flat, as assumed, that the real Rb uptake time is somewhat less than the Rb exposure time used, and that some of the Rb taken up has already left the cells, the total Rb uptake rate of surface and neck cells of 2.2 µmol·h -1 ·cm -2 is an underestimate and seems to be in the same order of magnitude as the parallel measured ouabain-sensitive Rb fluxes from the mucosal to the serosal side of about 1.5 and 2.5 µmol·h -1 ·cm -2 . Since Rb and K flux measurements yield similar values ( [35], Rechkemmer, unpublished data) it might be concluded that surface and neck cells are mainly responsible for K absorption.…”

β‐adrenergic stimulation of cellular K+ uptake in rat distal colon

“…Therefore, paracellular leakage could contribute to the higher colonic K + absorption during infancy. In this study we used the 86 Rb uptake assay, a well‐accepted method to determine the activity of K + transcellular transporters ( Tannen et al . 1986 , Diener et al .…”

“…The preparation of the distal colon and measurements of K + transport using 86 Rb as a marker of K + uptake ( Tannen et al . 1986 , Diener et al .…”

“…Knowledge on the hormonal regulation of K + transcellular transport in infant colon is scanty. Therefore, we aimed to estimate the effect of adrenergic agonists on K + uptake in rat distal colon during development, using the 86 Rb uptake method in intact colon as a marker for transcellular K + fluxes ( Tannen et al . 1986 , Diener et al .…”