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Evidence for gut factor in K⁺ homeostasis

Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California

Submitted 27 October 2006 ; accepted in final form 9 May 2007

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 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 overnight-fasted 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.

feedback control; feedforward control; potassium sensor; potassium excretion

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