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The cellular mechanisms responsible for rectal acidification in the desert locust, Schistocerca gregaria, were investigated in isolated recta mounted as flat sheets in modified Ussing chambers. Previous studies conducted in the nominal absence of exogenous CO2 and HCO3+ suggested that the acidification was due to a proton-secretory rather than bicarbonate-reabsorptive mechanism (Thomson, R.B., Speight, J.D., Phillips, J.E. 1988. J. Insect Physiol. 34:829-837). This conclusion was confirmed in the present study by demonstrating that metabolic CO2 could not contribute sufficient HCO3+ to the lumen to account for the rates of rectal acidification observed under the nominally CO2/HCO3+ free conditions used in these investigations.

Rates of luminal acidification (J(H)+) were completely unaffected by changes in contraluminal pH, but could be progressively reduced (and eventually abolished) by imposition of either transepithelial pH gradients (lumen acids) or transepithelial electrical gradients (lumen positive). Under short-circuit current conditions, the bulk of J(H+) was not dependent on Na+, K+, Cl+, Mg2+, or Ca2+ and was due to a primary electrogenic proton translocating mechanism located on the apical membrane. A small component (10-16%) of J(H+) measured under these conditions could be attributed to an apical amiloride-inhibitable Na+/H+ exchange mechanism.