The effect of furosemide on luminal sodium, chloride and potassium transport in the early distal tubule of Amphiuma kidney - Effects of potassium adaptation

Previous experiments in the early distal tubule of the doubly perfused kidney of Amphiuma demonstrated net reabsorption of potassium (K) which is reversed to net K secretion after K adaptation. Furthermore, it is known that this particular segment exhibits extensive chloride (Cl) net reabsorption which depends on the presence of sodium (Na) and which is inhibited by furosemide. In order to test for a possible interrelationship between NaCl and K transport, K activity in lumen and cell, transepithelial electrical potential difference, peritubular cell membrane potentials and volume reabsorption were measured in control animals and after K adaptation, in presence and absence of furosemide. In control animals the direction of net K transport is reversed from reabsorption to secretion upon addition of furosemide or following the removal of Cl from the tubular lumen. Volume reabsorption is inhibited by some 80%. In K adapted animals a similar inhibition of volume reabsorption is observed, however K secretion is not further enhanced. In control as well as in K-adpated animals intracellular K activities are still above electrochemical equilibrium after furosemide. The data suggest that a common transport system for Na, Cl and K is present in the luminal cell membrane which is inhibited by furosemide, K secretion observed in controls after furosemide and in K-adapted animals is driven by the cell to lumen electrochemical gradient for K across the K permeable luminal cell membrane. The shift of the luminal pump-leak system towards K secretion following K adaptation may be explained by an increase of the luminal K conductance and/or by a reduction of the activity of the luminal cotransport system. However, other mechanisms may also contribute to the observed phenomenon of K adaptation and cannot be ruled out at present.