| pubmed-article:137102 | pubmed:abstractText | Evaluation of a possible role of NaK-ATPase in transtubular sodium reabsorption is difficult, since ouabain doses that inhibit this enzyme system in vitro completely [1, 11], cannot be applied in vivo. Thus studies in the isolated perfused rat kidney were carried out [3, 11, 13, 15]. However, in this model, supramaximal doses of ouabain as used to block NaK-ATPase completely induced a potent vasoconstriction, which lowers the filtered load of sodium. Thus, a meaningful quantitative comparison of sodium transport in control and in experimental phases of ouabain inhibition has not been possible. At submaximal doses, in which filtered Na-loads are still comparable, transport activity was only reduced to approximately 50% [15]. In the following experiments we reinvestigated the relationship between inhibition of renal NaK-ATPase and the reduction of Na-reabsorption by ouabain under more appropriate conditions. Previously we have observed that verapamil (syn.: iproveratril, Isoptin), a Ca ion antagonist [2, 4, 6], effectively prevents autoregulation, and a fact which is pertinent for the present experiments, blocks this vasoconstrictive action of ouabain. Thus, using the Ca antagonist verapamil, it was possible to evaluate the inhibiting effect of this glycoside on renal sodium transport quantitatively without the hazards introduced by ouabain vasoconstriction which by the same token lowers filtered load. | lld:pubmed |
