Abstract
Summary
To substantiate our previous hypothesis in explanation of the inhibitory effect of EA, furosemide, and amiloride on mouse intestine, the intracellular potential, V mc, and transmural potential, V sm, of the intestinal mucosal epithelium were measured simultaneously with a 0.5-μm diameter microelectrode. It was found when glucose was present in the Ringer bathing solution, an average V sm of 22.5 ± 0.87 mV was recorded and V sm was 2.68 ± 0.09 mV. EA, furosemide, and amiloride at 0.5 mM produced an hyperpolarization of V mc and a reduction of V sm. The V mc increased to 34.8 ± 0.68, 31.9 ± 2.6, and 31.2 ± 0.92 mV, respectively. When the bathing fluid contained no glucose, the average V mc was 29.5 ± 0.53 mV and the average V sm was 1.28 ± 0.10 mV. Addition of EA in the glucose-free bathing media caused no significant change in V mc, but a decrease in V sm. However, addition of furosemide or amiloride did cause further hyperpolarizations of V mc, to 40.7 ± 0.64 and 39.8 ±1.2 mV, respectively. These results support our conclusion that EA mainly acts on the Na-glucose co-transport system and the other two diuretics act on the membrane conductance. The Ar-rhenius plots of the variations of V sm and V mc with temperature provide the calculation of the activation energies for the trans-mural and transmucosal potentials as 19.3 and 14.02 kcal/mole, respectively.
Get full access to this article
View all access options for this article.
