ABSTRACT
Electrophysiological and tracer flux techniques were used to study regulation of KCl reabsorption across locust recta. Physiologically high K+ levels (100 mmol 1−1) on the lumen side stimulated net 36C1 flux and reduced the theoretical energy cost of anion transport under open-circuit conductions.
The stimulation of short-circuit current (ISC, i.e. active Cl− absorption) by crude corpora cardiaca extracts (CC) was not dependent on exogenous Ca2+. Stimulations of Isc were greatly enhanced in the presence of theophylline, indicating that the rate of synthesis of cAMP is increased by CC extracts. High CC levels lowered transepithelial resistance (Rt), suggesting that chloride transport stimulating hormone (CTSH) regulates both active Cl− absorption and counter-ion (K+) permeability.
High mucosal osmolarity or K+ concentration decreased Isc. and caused a disproportionately large increase in Rt, consistent with a decrease in the shunt (K+) conductance. Measurements of relative mucosal-to-serosal membrane resistance confirmed that high mucosal K+ levels reduced apical membrane conductance. Lowering mucosal pH to values observed in vivo at the end of resorptive cycles also inhibited Isc, apparently without affecting K+ permeability.