Luminal signal in tubuloglomerular feedback: what about potassium?

Evidence suggests that a minimal luminal [K+] is required to elicit a full tubuloglomerular feedback (TGF) response, consistent with transmission of the TGF signal across the macula densa (MD) via the Na+-2Cl(-)-K+ cotransporter. Furthermore, it appears that luminal [K+] at the MD is close to the K+ affinity of the Na+-2Cl(-)-K+ cotransporter and changes in response to altering late proximal tubular flow rate (VLP), that is, a maneuver that induces a TGF response. These findings suggest that luminal [K+] (besides [Cl-]) could be rate limiting in TGF. In the thick ascending limb of Henle's loop (TALH), most of the luminal K+ is derived from recycling across the apical tubular membrane. Because changing VLP causes relatively greater alterations in the absolute Na+ and Cl- delivery to Henle's loop than in K+ load, the parallel changes of VLP and luminal [K+] at the MD, despite significant alteration in K+-dependent reabsorption of Na+ and Cl- via the Na+-2Cl(-)-K+ cotransporter, imply a transport-dependent adaptation of K+ recycling in TALH.