The mechanism of the urinary concentrating defect in potassium deficient rats.

Abstract

The mechanism of the defect in urinary concentrating capacity in potassium deficiency was investigated by measuring solute-free water reabsorption (\(T_{{\text{H}}_{\text{2}} {\text{O}}}^{\text{C}}\)) in normal and hypokalemic rats undergoing mannitol diuresis. Since potassium-deficiency markedly lowered glomerular filtration rate (GFR), \(T_{{\text{H}}_{\text{2}} {\text{O}}}^{\text{C}}\) was examined in normal rats whose GFR had been comparably reduced either acutely by aortic constriction or chronically by feeding a salt- and protein-free diet. By calculating the volume of filtrate delivered to the loop of Henle from the GFR and Cosmit was found that in normal rats \(T_{{\text{H}}_{\text{2}} {\text{O}}}^{\text{C}}\) was linearly related to volume delivery. At each level of volume delivery to the loop hypokalemic rats formed about half the normal amount of \(T_{{\text{H}}_{\text{2}} {\text{O}}}^{\text{C}}\). Decreased solute delivery to the loop of Henle, therefore, cannot be the cause of the concentrating defect in hypokalemia. It is concluded, therefore, that the impaired concentrating capacity in potassium deficiency results from defective sodium transport in the ascending limb of Henle's loop, so that at any level of sodium delivery to the loop less sodium is transported into the medulla and therefore less \(T_{{\text{H}}_{\text{2}} {\text{O}}}^{\text{C}}\) is generated.