Cellular Mechanisms and Control of KCL Absorption in Insect Hindgut

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Abstract
The hindgut of the desert locust possesses an unusual chloride transport system. The isolated locust rectum absorbs chloride from the mucosal (lumen) to the serosal (haemolymph) side at a rate which is equal to the short-circuit current (Isc). Net chloride transport persists in nominally Na-free or HCO3(CO2)-free saline, is insensitive to normal inhibitors of NaCl co-transport and anion exchange, and is independent of the net electrochemical gradient for sodium across the apical membrane. However, active chloride transport is strongly dependent on mucosal potassium (K2 = 5·3mm-K). Chloride entry across the apical membrane is active, whereas the net electrochemical gradient across the basal membrane favours passive Cl exit from the cell. Although mucosal potassium directly stimulates ‘uphill’ chloride entry, there is no evidence for coupled KCL co-transport, nor would co-entry with potassium be advantageous energetically. Net chloride absorption and IK are stimulated by a peptide hormone from the central nervous system which acts via cyclic-AMP. Cyclic-AMP increases Isc and approximately 1000% and transepithelial conductance (Gt) ˜100%. Approximately half of the ΔGt during stimulation results from increased Cl conductance at the basal cell border. This increase is also reflected in a shift of the basal membrane e.m.f. towards the Nemst potential for chloride. The remainder of the cAMP-induced ΔGt is due to an elevation of apical membrane K conductance, which causes a 400% increase in transepithelial potassium permeability as estimated by radiotracer diffusion. Because of this stimulation of K conductance, potassium serves as the principal counterion for active chloride transport under open-circuit conditions. Very high luminal levels of K oppose the stimulatory actions of cAMP on active Cl transport and K conductance. These and other results have been incorporated into a cellular model for KCL absorption across this insect epithelium.