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-adapted 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.