1. From two lines of evidence, we conclude that the potassium transport gives rise directly to the midgut potential, i.e. that the active potassium transport mechanism is electrogenic.
2. First, diffusion potentials of neither potassium, sodium, magnesium, calcium, nor chloride could give rise to the large midgut potential if values for tissue concentrations are accepted for their respective activities in the epithelium.
3. Secondly, no externally added cation other than potassium is required to sustain either the potential or short circuit current, no specific anion is required, and no metabolic ion is known to be produced in sufficient amount to act as a counter ion for potassium in a non-electrogenic process.
4. Changes in the concentration of potassium on the blood-side of the midgut always lead to changes in potential in the direction predicted by the Nernst equation. Moreover, a tenfold change in potassium concentration leads to the expected 59 mV. potential change provided that the prior midgut potential is at least 130 mV. This effect could be attributed either to the stimulation of an electrogenic potassium pump or to a potassium diffusion potential across the blood-side barrier.