An acute increase of peritubular K stimulates K transport through cell pathways of CCT

In this study, we have investigated net transport and electrical properties of isolated perfused cortical collecting ducts of control and DOCA-treated rabbits to clarify the cell mechanism for secreting K on an acute increase of peritubular K concentration. Raising bath K in control experiments caused an increase in net K secretion (-J(K)) and net Na absorption (J(Na)). Barium (5 mM), a known blocker of basolateral K conductance, added to the bath had no effect on this transport stimulation. In the presence of luminal Ba (5 mM)- J(K) was reduced to zero, but J(Na) was unaltered. When bath K was increased -J(K) increased to a value slightly greater than zero, but not different from the predicted passive flux through the paracellular pathway. In tubules of DOCA-treated rabbits, raising K in the bath increased -J(K) and J(Na). The observed stimulation of -J(K) was blunted in the presence of Ba in the bath, whereas the increase in J(Na) remained the same. Thus, in DOCA-treated tubules, Ba in the bath significantly attenuated the increase in K secretion without affecting the transport stimulation of J(Na). When Ba was added to the perfusate and bath K increased, -J(K), which was initially 22.1, increased to 36.4 pmol · mm^-1 · min^-1 ·. Thus a 'Ba-insensitive' pathway became more evident in CCTs from DOCA-treated rabbits. We conclude the following: 1) in control tubules, raising bath K causes an increase in K secretion primarily by stimulating the rate of turnover of the basolateral membrane bound Na-K pump; 2) in DOCA-treated tubules, an acute increase in bath K stimulated K secretion via two basolateral membrane pathways, the Na-K pump and a Ba-sensitive pathway; 3) luminal Ba blocks K transport to near zero in control tubules but does not completely inhibit K transport in DOCA-treated tubules.