Microelectrode study of K+ accumulation by tight epithelia: II. Effect of inhibiting transepithelial Na+ transport on reaccumulation following depletion

Abstract

The effects of restoring serosal potassium to potassium-depleted toad urinary bladders have been re-examined using double-barrelled microelectrodes. The data confirm the existence of a time-lag phenomenon, a dissociation between potassium reaccumulation and restoration of short-circuit current. Returning serosal potassium stimulates an increase in intracellular potassium activity 21-26 min before any increase can be detected in short-circuit current. The reaccumulation of potassium has been further studied using split frog skin, a far more suitable preparation for electrophysiologic study than toad bladder. Under baseline short-circuited conditions, potassium is accumulated against an electrochemical gradient of 22 +/- 4 mV. Reaccumulation of potassium by potassium-depleted tissues can be blocked by inhibiting the Na,K-exchange pump with high concentrations of ouabain. On the other hand, blocking apical sodium entry by the addition of 10(-4) M amiloride to the outer bathing medium does not interfere with reaccumulation of potassium. The data support the concept that the time-lag phenomenon of toad bladder reflects stimulation of potassium reaccumulation by the sodium pump in exchange for the extrusion of excess cell sodium collected during the period of potassium depletion. This reaccumulation of potassium can proceed before the entry of significant added amounts of sodium across the apical plasma membrane.

Intracellular potassium activity and the role of potassium in transepithelial salt transport in the human reabsorptive sweat duct

“…The low cell potentials in RSD [24] as compared to both the K--equilibrium potentials (Table 2) and the cell potentials of other epithelia [7,28] seems to be due to a relatively low K ~ conductance rather than to an absence of K § conductance in the BLM based on several pieces of evidence. First, increasing the K + concentration 10-fold in the bath elevated [K+]i and depolarized V~ (Table 4).…”

“…P > 0.05. b Since the lumen and contraluminal bath contain equimolar K + concentrations, the E k represents the value of K + equilibrium potentials at APM and BLM. [28], proximal tubules [8] and urinary bladder [7]. It is important to note that in all of the above epithelia, Vb is much closer to the K + equilibrium potential (Ek) across the BLM suggesting that in those epithelia the EMF at the BLM (Eb) is predominantly determined by transmembrane K + distribution.…”

“…Until now there has been almost no information available on the [K+]i, mechanism(s) of K + uptake, or the role of K + transport in the transepithelial salt movement of human reabsorptive sweat duct (RSD). In addition, RSD is a unique tissue compared with many NaC1 absorbing epithelia, such as frog skin [13], gall bladder [11], and urinary bladder [7], in that the RSD has low cell membrane electrical potentials [24] and an extremely high transepithelial C1-conductance [22,25,26]. We do not know the physiological basis of such low cellular potentials [24], but several factors which could be responsible for the low potentials in RSD include (i) a very small ratio of transmembrane K + distribution ([K+]~ may be very low as compared to other epithelia), (ii) a small or absent K + conductance in the BLM ~ and APM, (iii) membrane electromotive force (EMF) is generated by an ion other than K + (possibly C1-), and (iv) a large paraceUular current loop in the RSD which shunts a more negative K+-EMF across the BLM to a more positive apical EMF [24][25][26].…”

“…However, there are wide differences among various epithelia with regard to (i) the intracellular K + activity [1,7,17], (ii) the mechanisms responsible for [K+],. accumulation such as the Na+/K + pump and KC1 cotransport [1,18], and (iii) the K +-conductance properties of apical and basolateral membranes [12,20].…”