KCl Reabsorption by the Lower Malpighian Tubule of Rhodnius prolixus: Inhibition by Cl super(-) Channel Blockers and Acetazolamide

Iono- and osmoregulation by the blood-feeding hemipteran Rhodnius prolixus involves coordinated actions of the upper and lower Malpighian tubules. The upper tubule secretes ions (Na super(+), K super(+), Cl super(-)) and water, whereas the lower tubule reabsorbs K super(+) and Cl super(-) but not water. The extent of KCl reabsorption by the lower tubule in vitro was monitored by ion-selective microelectrode measurement of Cl super(-) and/or K super(+) concentration in droplets of fluid secreted by Malpighian tubules isolated under oil. An earlier study proposed that K super(+) reabsorption involves an omeprazole-sensitive apical K super(+)/H super(+) ATPase and Ba super(2+)-sensitive basolateral K super(+) channels. This paper examines the effects acetazolamide and of compounds that inhibit chloride channels, Cl super(-)/HCO sub(3) super(-) exchangers and Na super(+)/K super(+)/2Cl super(-) or K super(+)/Cl super(-) co-transporters. The results suggest that Cl super(-) reabsorption is inhibited by acetazolamide and by Cl super(-) channel blockers, including diphenylamine-2-carboxylate(DPC) and 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), but not by compounds that block Na super(+)/K super(+)/Cl super(-) and K super(+)/Cl super(-) co-transporters. Measurements of transepithelial potential and basolateral membrane potential during changes in bathing saline chloride concentration indicate the presence of DPC- and NPPB-sensitive chloride channels in the basolateral membrane. A working hypothesis of ion movements during KCl reabsorption proposes that Cl super(-) moves from lumen to cell through a stilbene-insensitive Cl super(-)/HCO sub(3) super(-) exchanger and then exits the cell through basolateral Cl super(-) channels.