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This Article Full Text Full Text (PDF) All Versions of this Article: 572/2/493    most recent jphysiol.2005.101576v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cheema-Dhadli, S. Articles by Halperin, M. L. Search for Related Content PubMed PubMed Citation Articles by Cheema-Dhadli, S. Articles by Halperin, M. L. Related Collections Renal and Endocrine

¹ Renal Division, St. Michael's Hospital, University of Toronto, Toronto, Canada
² Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, R.O.C.

Control mechanisms for potassium (K⁺) excretion in humans developed in Palaeolithic times when diets were sodium poor and episodically K⁺ rich. Nevertheless, our understanding of the regulation of K⁺ excretion comes from experiments in rats with large sodium and K⁺ intakes. Our objective was to identify how K⁺ excretion was regulated when rats consumed a low NaCl diet to reflect Palaeolithic conditions. Rats that were given mineralocorticoids plus either NaCl, mannitol, or NaHCO₃ had a small kaliuresis. In contrast, KCl load induced a large kaliuresis and a near-maximal luminal [K⁺] in the terminal cortical collecting duct ([K⁺]_CCD). The time course of events was important. The rise in the [K⁺]_CCD was prompt, but the initial kaliuresis was only modest. Over the next 4 h, kaliuresis increased markedly due solely to a higher calculated distal flow rate, which appeared to be due to diminished reabsorption of NaCl in the loop of Henle; of note, the measured papillary [K⁺] rose. In summary, the increase in the [K⁺]_CCD in rats given KCl is likely to be due to an increase in the number of luminal K⁺ channels rather than to mechanisms that are known to induce a lumen-negative voltage in cortical distal nephron segments. The higher distal flow rate might be due to a higher interstitial [K⁺], which inhibited NaCl reabsorption in the loop of Henle. Thus, to understand which of the potential control mechanisms are operating, one must look very closely at the conditions imposed by the experimental setting.

(Received 7 December 2005; accepted after revision 27 January 2006; first published online 2 February 2006)
Corresponding author M. L. Halperin: Division of Nephrology, Street Michael's Hospital Annex, 38 Shuter St, Toronto, Ontario, Canada, M5B 1A6. Email: mitchell.halperin{at}utoronto.ca

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