Effects of the potassium channel blocker barium on sodium and potassium transport in the rat loop of Henle in vivo

In vitro evidence suggests that the 'recycling' of K+ ions through luminal K+ channels in the thick ascending limb of the loop of Henle (TALH) is essential for the normal operation of the luminal Na+-K+-2Cl(-) co-transporter. In the present study these channels were investigated in vivo by perfusing superficial loops of Henle in anaesthetised rats with and without the K+ channel blocker barium. Using a standard perfusate, intraluminal barium (5 mmol 1(-1)) reduced sodium reabsorption (J(Na)) from 1887 +/- 50 to 1319 +/- 53 pmol min(-1) (P < 0.001). When the experiment was repeated using a low-Na+ perfusate, designed to inhibit reabsorption in the pars recta (the initial segment of the loop of Henle), a similar reduction in J(Na) was observed (from 698 +/- 47 to 149 +/- 23 pmol min(-1), P < 0.001), strongly suggesting that the effect of barium is localised to the TALK The magnitude of the reduction in J(Na) during blockade of K+ channels confirms the importance of K+ recycling in facilitating Na+ reabsorption in the TALH in vivo. However, the reduction in J(Na) was not associated with a fall in the K+ concentration of the fluid collected at the early distal tubule. When bumetanide, an inhibitor of the Na+-K+-2Cl(-) co-transporter, was included in the low-Na+ perfusate, net K+ secretion was observed. Addition of barium to this perfusate reduced, but did not abolish, the secretion, suggesting that bumetanide-induced K+ secretion results partly from paracellular transport.