Evidence for gut factor in K+ homeostasis

We tested the hypothesis that K+ intake is sensed by putative K+ sensors in the splanchnic areas, and renal K+ handling is regulated by this signal. K+ was infused for 2 h into overnight- fasted rats via the jugular vein ( systemic infusion), hepatic portal vein ( intraportal infusion), or stomach ( intragastric infusion) ( n = 5 each), and plasma K+ concentration ([ K+]) and renal K+ excretion were measured during the 2-h preinfusion, 2- h K+ infusion, and 3- h washout periods. During systemic K+ infusion, plasma [ K+] increased by similar to 1.3 mM ( P < 0.05), and, on cessation of the K+ infusion, plasma [ K+] fell to the preinfusion level within 1 - 2 h. Renal K+ excretion changed in proportion to the changes in plasma [ K+]. During intraportal or intragastric K+ infusion, plasma [ K+] and renal K+ excretion profiles were similar to those with systemic infusion. The effects of K+ infusions via the different routes ( n = 5 or 6 each) were also studied during simultaneous feeding of overnightfasted rats with a K+- deficient diet. During the meal, intraportal infusion resulted in increases in plasma [ K+] similar to those with the systemic K+ infusion, while intragastric K+ infusion did not significantly increase plasma [ K+]. Thus, when the intragastric K+ infusion was combined with a meal, there was marked enhancement of clearance of the K+ infused, which was associated with an apparent increase in renal efficiency of K+ excretion. These data suggest that there may be a gut factor that enhances renal efficiency of K+ excretion during meal ( or dietary K+) intake.