NDLI: Mechanisms of acute natriuresis in normal humans on low sodium diet

Content Provider	PubMed Central
Author	Rasmussen, M. S. Simonsen, J. A. Sandgaard, N. C. F. Høilund-carlsen, P. F. Bie, P.
Copyright Year	2003
Abstract	This study evaluates the relative importance of several mechanisms possibly involved in the natriuresis elicited by slow sodium loading, i.e. the renin-angiotensin-aldosterone system (RAAS), mean arterial blood pressure (MAP), glomerular filtration rate (GFR), atrial natriuretic peptide (ANP), oxytocin and nitric oxide (NO). Eight seated subjects on standardised sodium intake (30 mmol NaCl day−1) received isotonic saline intravenously (NaLoading: 20 μmol Na+ kg−1 min−1 or ≈11 ml min−1 for 240 min). NaLoading did not change MAP or GFR (by clearance of 51Cr-EDTA). Significant natriuresis occurred within 1 h (from 9 ± 3 to 13 ± 2 μmol min−1). A 6-fold increase was found during the last hour of infusion as plasma renin activity, angiotensin II (ANGII) and aldosterone decreased markedly. Sodium excretion continued to increase after NaLoading. During NaLoading, plasma renin activity and ANGII were linearly related (R = 0.997) as were ANGII and aldosterone (R = 0.999). The slopes were 0.40 pm ANGII (mi.u. renin activity)−1 and 22 pm aldosterone (pm ANGII)−1. Plasma ANP and oxytocin remained unchanged, as did the urinary excretion rates of cGMP and NO metabolites (NOx). In conclusion, sodium excretion may increase 7-fold without changes in MAP, GFR, plasma ANP, plasma oxytocin, and cGMP- and NOx excretion, but concomitant with marked decreases in circulating RAAS components. The immediate renal response to sodium excess appears to be fading of ANGII-mediated tubular sodium reabsorption. Subsequently the decrease in aldosterone may become important.
Related Links	http://dx.doi.org/10.1113/jphysiol.2002.027425
Ending Page	603
Page Count	13
Starting Page	591
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 2
Volume Number	546
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2003-01-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

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