Calcium deprivation increases salt intake
Autor: | J. Schulkin, M. G. Tordoff, P. M. Ulrich |
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Rok vydání: | 1990 |
Předmět: |
Male
Sucrose medicine.medical_specialty Physiology Sodium media_common.quotation_subject Drinking chemistry.chemical_element Sodium Chloride Calcium Citric Acid Excretion Food Preferences chemistry.chemical_compound Saccharin Physiology (medical) Internal medicine medicine Animals Citrates Salt intake media_common Aldosterone Osmolar Concentration Rats Inbred Strains Appetite Animal Feed Rats Calcium Dietary Solutions Endocrinology chemistry Sucrose octaacetate |
Zdroj: | Scopus-Elsevier |
ISSN: | 1522-1490 0363-6119 |
DOI: | 10.1152/ajpregu.1990.259.3.r411 |
Popis: | Relative to rats fed chow or semisynthetic control diet, rats fed Ca2(+)-deficient diet increased daily "spontaneous" intake of 0.3 M NaCl solution by as much as eightfold. Intake of 0.3 M NaCl increased in monotonic relationship to the severity of Ca2+ deficiency, which was manipulated by both duration of depletion (0-32 days) and dietary Ca2+ content (0-50 mmol/kg Ca2+). The increased intake was specific to either Na+ or saltiness; relative to controls, Ca2(+)-deprived rats drank more of a wide range of NaCl solutions (0.05-0.50 M) but the same volume of 0.37 mM sucrose octaacetate (bitter), slightly more 2.5 mM citrate (sour), and significantly less 2.5 mM saccharin (sweet). Although urine volume of Ca2(+)-deprived rats was increased, total Na+ excretion was slightly decreased. Adrenal weights, hematocrit, and plasma concentrations of Na+, aldosterone, and angiotensin I were all normal. These results reveal that Ca2+ deficiency increases NaCl intake and thus challenge the notion that salt appetite is a specific response to perturbed Na+ homeostasis. |
Databáze: | OpenAIRE |
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