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Research Article Free access | 10.1172/JCI107743
1Hypertension-Endocrine Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
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1Hypertension-Endocrine Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
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1Hypertension-Endocrine Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
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1Hypertension-Endocrine Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
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1Hypertension-Endocrine Branch, National Heart and Lung Institute, National Institutes of Health, Bethesda, Maryland 20014
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Published July 1, 1974 - More info
The effects of dietary sodium and of saline infusion on urinary dopamine and norepinephrine and on the relationship of these catecholamines to adrenergic activity were determined. In seven normal subjects on a 9-meq sodium intake, urinary dopamine and norepinephrine were 136±18 (SE) and 37.4±5.3 μg/day, respectively. When sodium intake was increased to 209 or 259 meq/day, urinary dopamine increased to 195±20 μg/day (P<0.01) whereas urinary norepinephrine decreased to 21.1±3.0 μg/day (P<0.01). Infusion of saline in seven subjects increased sodium excretion and urinary dopamine (from 2.18±0.22 to 2.79±0.19 μg/20 min, P<0.01), but decreased plasma dopamine-β-hydroxylase by 33% and urinary norepinephrine insignificantly. The clearance of inulin and p-aminohippurate did not change significantly and filtration fraction was the same. The data indicate that an increase in dietary sodium or infusion of saline results in an apparent decrease in adrenergic activity and an increase in urinary dopamine. Dopamine excretion would thus appear to relate inversely to adrenergic activity and to parallel sodium excretion. These findings suggest a possible role for dopamine and norepinephrine in the regulation of renal sodium excretion.