Contributions of K+:Cl- cotransport and Na+/K+-ATPase to basolateral ion transport in malpighian tubules of Drosophila melanogaster

Linton, S. and O'Donnell, M. J. 1999, Contributions of K+:Cl- cotransport and Na+/K+-ATPase to basolateral ion transport in malpighian tubules of Drosophila melanogaster, Journal of experimental biology, vol. 202, no. 11, pp. 1561-1570.

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Title Contributions of K+:Cl- cotransport and Na+/K+-ATPase to basolateral ion transport in malpighian tubules of Drosophila melanogaster
Author(s) Linton, S.ORCID iD for Linton, S.
O'Donnell, M. J.
Journal name Journal of experimental biology
Volume number 202
Issue number 11
Start page 1561
End page 1570
Total pages 10
Publisher Company of Biologists
Place of publication Cambridge, Eng.
Publication date 1999-06
ISSN 0022-0949
Summary Mechanisms of Na+ and K+ transport across the basolateral membrane of isolated Malpighian tubules of Drosophila melanogaster were studied by examining the effects of ion substitution and putative inhibitors of specific ion transporters on fluid secretion rates, basolateral membrane potential and secreted fluid cation composition. Inhibition of fluid secretion by [(dihydroindenyl)oxy]alkanoic acid (DIOA) and bumetanide (10-4 mol l-1) suggested that a K+:Cl- cotransporter is the main route for K+ entry into the principal cells of the tubules. Differences in the effects of bumetanide on fluxes of K+ and Na+ are inconsistent with effects upon a basolateral Na+:K+:2Cl- cotransporter. Large differences in electrical potential across apical (>100 mV, lumen positive) and basolateral (<60 mV, cell negative) cell membranes suggest that a favourable electrochemical gradient for Cl- entry into the Cell may be used to drive K+ into the cell against its electrochemical gradient, via a DIOA-sensitive K+:Cl- cotransporter. A Na+/K+-ATPase was also present in the basolateral membrane of the Malpighian tubules. Addition of 10-5 to 10-3 mol l-1 ouabain to unstimulated tubules depolarized the basolateral potential, increased the Na+ concentration of the secreted fluid by 50-73% and increased the fluid secretion rate by 10-19%, consistent with an increased availability of intracellular Na+. We suggest that an apical vacuolar-type H+-ATPase and a basolateral Na+/K+ATPase are both stimulated by cyclic AMP. In cyclic-AMP-stimulated tubules, K+ entry is stimulated by the increase in the apical membrane potential, which drives K+:Cl- cotransport at a faster rate, and by the stimulation of the Na+/K+-ATPase. Fluid secretion by cyclic-AMP-stimulated tubules was reduced by 26% in the presence of ouabain, suggesting that the Na+/K+-ATPase plays a minor role in K+ entry into the tubule cells. Malpighian tubules secreted a Na+-rich (150 mmol l-1) fluid at high rates when bathed in K+-free amino-acid-replete saline (AARS). Secretion in K+-free AARS was inhibited by amiloride and bafilomycin A1, but not by bumetanide or hydrochlorothiazide, which inhibit Na+:Cl- cotransport. There was no evidence for a Na+ conductance in the basolateral membrane of unstimulated or cyclic-AMP-stimulated tubules. Possible mechanisms of Na+ entry into the tubule cells include cotransport with organic solutes such as amino acids and glucose.
Language eng
Indigenous content off
Field of Research 06 Biological Sciences
11 Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©1999, The Company of Biologists Limited
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