Mechanisms and properties of sodium transport in locust rectum

Abstract

Steady-state fluxes of 22Na+ were measured as a function of external Na+ concentration across locust recta mounted as flat sheets under short-circuit conditions. A net flux [Formula: see text] at all concentrations confirmed that absorption was an active process obeying Michaelis–Menten kinetics with Kt of 17 mM and Vmax of 1.5 to 2.5 μequiv. cm−2 h−1. [Formula: see text] was not affected by cAMP, was independent of external Cl− levels and stimulated short-circuit current (i.e., Cl− transport), and was partially inhibited by amiloride and ouabain but not by vanadate. Using intracellular electrodes, a small Na+ conductance that was not due to cotransport with organic substrates was identified in the apical plasma membrane. A semiquantitative model for Na+ absorption in this epithelium is proposed. We surveyed the locust neurosecretory system for water-soluble factors that might control rectal Na+ reabsorption.