Mechanisms of K+ uptake across the basal membrane of malpighian tubules of Formica polyctena: the effect of ions and inhibitors

Abstract

In the presence of 6 mmol l-1 Ba2+, known to block the K+ channels in the basal membrane, a rise in bath [K+] ([K+]bl) induced an increase in intracellular K+ concentration ([K+]i) similar in amount and in time course to that obtained in the absence of Ba2+. The presence of active and passive (other than through K+ channels) K+ uptake mechanisms across the basal membrane was investigated in different bath K+ concentrations. Dihydro-ouabain (10(-3) mol l-1), a blocker of the Na+/K(+)-ATPase, tested in low bath [K+], and Sch28080 (10(-4) mol l-1), a K+/H(+)-ATPase inhibitor, were without effect on fluid secretion. Dihydro-ouabain was also without effect on electrical potential differences either in the absence or in the presence of Ba2+. Vanadate (10(-3) mol l-1), in contrast, strongly reduced fluid secretion not only in control solution but also in high-K+, Na(+)-free medium and reduced the transepithelial and the apical membrane potential differences but not the basal membrane potential difference of [K+]i. Omitting Na+ from the bathing medium, replacing Cl- by Br- or applying bumetanide (10(-5) mol l-1) inhibited fluid secretion only in a low-K+ (10 mmol l-1) medium. In 51 mmol l-1 [K+]bl, omitting Na+ was without effect and 10(-4) mol l-1 bumetanide was needed to inhibit secretion. Replacing Cl- by Br- stimulated fluid secretion at this K+ concentration. Bumetanide (10(-4) mol l-1) had no effect in 113 mmol l-1 [K+]bl. Bumetanide (10(-4) mol l-1) in 51 mmol l-1 [K+]bl did not affect membrane potentials, did not lower [K+]i and did not affect the rise in [K+]i observed on an increase in [K+]bl. The results were summarized in a model proposing that K+ channels play a dominant role in high-K+ (113 mmol l-1) bathing medium. A K+/Cl- cotransporter may become more important in 51 mmol l-1 [K+]bl and a K+/Na+/2Cl- cotransporter may gain in importance in 10 mmol l-1 [K+]bl. Active mechanisms for K+ uptake across the basal membrane seem to play no detectable role in sustaining fluid secretion. The response to vanadate might be due to an effect on the apical electrogenic H+ pump.