| Gut sensing of dietary K⁺ intake increases renal K⁺excretion. | |
| | |
MedLine Citation:
|
PMID: 21543632 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
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:
|
Ki-Sook Oh; Young Taek Oh; Sang-Wook Kim; Toshihiro Kita; Insug Kang; Jang H Youn |
Publication Detail:
|
Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-05-04 |
Journal Detail:
|
Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: 301 ISSN: 1522-1490 ISO Abbreviation: Am. J. Physiol. Regul. Integr. Comp. Physiol. Publication Date: 2011 Aug |
Date Detail:
|
Created Date: 2011-08-03 Completed Date: 2011-10-18 Revised Date: 2012-09-25 |
Medline Journal Info:
|
Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: United States |
Other Details:
|
Languages: eng Pagination: R421-9 Citation Subset: IM |
Affiliation:
|
Department of Physiology and Biophysics, University of Southern California, Keck School of Medicine, Los Angeles, California 90089-9142, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Aldosterone
/
blood,
metabolism Amiloride / pharmacology Animals Blood Glucose Gastrointestinal Tract / metabolism* Gene Expression Regulation / physiology Kidney / metabolism* Male Pituitary Hormones / genetics, metabolism Postprandial Period Potassium / blood*, metabolism* Potassium, Dietary / metabolism* Rats Rats, Wistar Sodium / blood Sodium Channel Blockers / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
|
DK 080233/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
|
0/Blood Glucose; 0/Pituitary Hormones; 0/Potassium, Dietary; 0/Sodium Channel Blockers; 2609-46-3/Amiloride; 52-39-1/Aldosterone; 7440-09-7/Potassium; 7440-23-5/Sodium |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Relationship between surface area of nonperfused myocardium and extravascular extraction of contrast...
Next Document: mu-Opioid receptor stimulation in the nucleus accumbens elevates fatty tastant intake by increasing ...