title: Mechanism and control of salt absorption in locust rectum.
abstract: The rectum is the main reabsorptive site in the excretory system of locusts. The primary urine entering this organ from the Malpighian tubules is rich in K+ (140 mM) and Cl- (90 mM), and most of this fluid is normally reabsorbed. Fluid and active Cl- reabsorption in the rectum are regulated by neuropeptide hormones from the corpus cardiacum. We have studied the mechanism of KCl reabsorption using voltage clamp, tracers, double-barreled ion-sensitive microelectrodes, and ion substitutions. Locust Cl- absorption differs from vertebrate systems in that it is not dependent on Na+ or HCO-3/CO2, and it is insensitive to normal inhibitors of Cl- transport. Entry of Cl- into rectal cells is active, electrogenic, and stimulated by luminal K+. This cation substantially increases the electrochemical gradient across the apical membrane against which Cl- is pumped; therefore K+ does not act solely and indirectly by electrical coupling. Kinetic studies also suggest that K+ activates the Cl- pump. Consequently at least two levels of control are exerted during cAMP stimulation; K+ permeability of the epithelium and the transepithelial potential generated by active Cl- transport both increase. The enhanced net K+ absorption from the lumen side after stimulation is largely passive, being electrically coupled to Cl- transport. However, this general increase in KCl absorption is "fine tuned" by K+ itself, through its direct effect on the Cl- pump.
mesh_terms: D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D001692:Biological Transport; D002712:Chlorides / Q000378:metabolism; D006110:Grasshoppers / Q000378:metabolism*; D007408:Intestinal Absorption; D007700:Kinetics; D011188:Potassium / Q000378:metabolism; D012007:Rectum / Q000378:metabolism*; D012492:Salts / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism
chemical_list: D001639:Bicarbonates; D002712:Chlorides; D012492:Salts; D012964:Sodium; D011188:Potassium