title: Gut sensing of dietary K⁺ intake increases renal K⁺excretion.
abstract: Dietary K(+) intake may increase renal K(+) excretion via increasing plasma [K(+)] and/or activating a mechanism independent of plasma [K(+)]. We evaluated these mechanisms during normal dietary K(+) intake. After an overnight fast, [K(+)] and renal K(+) excretion were measured in rats fed either 0% K(+) or the normal 1% K(+) diet. In a third group, rats were fed with the 0% K(+) diet, and KCl was infused to match plasma [K(+)] profile to that of the 1% K(+) diet group. The 1% K(+) feeding significantly increased renal K(+) excretion, associated with slight increases in plasma [K(+)], whereas the 0% K(+) diet decreased K(+) excretion, associated with decreases in plasma [K(+)]. In the KCl-infused 0% K(+) diet group, renal K(+) excretion was significantly less than that of the 1% K(+) group, despite matched plasma [K(+)] profiles. We also examined whether dietary K(+) alters plasma profiles of gut peptides, such as guanylin, uroguanylin, glucagon-like peptide 1, and glucose-dependent insulinotropic polypeptide, pituitary peptides, such as AVP, α-MSH, and γ-MSH, or aldosterone. Our data do not support a role for these hormones in the stimulation of renal K(+) excretion during normal K(+) intake. In conclusion, postprandial increases in renal K(+) excretion cannot be fully accounted for by changes in plasma [K(+)] and that gut sensing of dietary K(+) is an important component of the regulation of renal K(+) excretion. Our studies on gut and pituitary peptide hormones suggest that there may be previously unknown humoral factors that stimulate renal K(+) excretion during dietary K(+) intake.
authors.affiliation: Department of Physiology and Biophysics, University of Southern California, Keck School of Medicine, Los Angeles, California 90089-9142, USA.
authors.forename: Ki-Sook
authors.initials: KS
authors.lastname: Oh
authors.forename: Young Taek
authors.initials: YT
authors.lastname: Oh
authors.forename: Sang-Wook
authors.initials: SW
authors.lastname: Kim
authors.forename: Toshihiro
authors.initials: T
authors.lastname: Kita
authors.forename: Insug
authors.initials: I
authors.lastname: Kang
authors.forename: Jang H
authors.initials: JH
authors.lastname: Youn
mesh_terms: D000450:Aldosterone / Q000097:blood / Q000378:metabolism; D000584:Amiloride / Q000494:pharmacology; D000818:Animals; D001786:Blood Glucose; D041981:Gastrointestinal Tract / Q000378:metabolism*; D005786:Gene Expression Regulation / Q000502:physiology; D007668:Kidney / Q000378:metabolism*; D008297:Male; D010907:Pituitary Hormones / Q000235:genetics / Q000378:metabolism; D019518:Postprandial Period; D011188:Potassium / Q000097:blood* / Q000378:metabolism*; D017419:Potassium, Dietary / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000097:blood; D026941:Sodium Channel Blockers / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D010907:Pituitary Hormones; D017419:Potassium, Dietary; D026941:Sodium Channel Blockers; D000450:Aldosterone; D000584:Amiloride; D012964:Sodium; D011188:Potassium