Mechanisms of acute natriuresis in normal humans on low sodium diet
| Autor: | Poul Flemming Høilund-Carlsen, N. C. F. Sandgaard, Peter Bie, Jane Angel Simonsen, Mona Sommer Rasmussen |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2003 |
| Předmět: |
Adult
Male medicine.medical_specialty Physiology Sodium food.diet chemistry.chemical_element Natriuresis Low sodium diet Oxytocin Plasma renin activity chemistry.chemical_compound food Atrial natriuretic peptide Reference Values Internal medicine medicine Humans Aldosterone Renal sodium reabsorption Osmolar Concentration Hemodynamics Original Articles Blood Proteins Diet Sodium-Restricted Angiotensin II Arginine Vasopressin Endocrinology chemistry cardiovascular system hormones hormone substitutes and hormone antagonists Atrial Natriuretic Factor Glomerular Filtration Rate |
| Zdroj: | Rasmussen, M S, Simonsen, J A, Sandgaard, N C F, Høilund-Carlsen, P F & Bie. P. 2003, ' Mechanisms of acute natriuresis in normal humans on low sodium diet ', Journal of Physiology, vol. 546, pp. 591-603 . University of Southern Denmark |
| Popis: | 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 micromol Na(+) kg(-1) min(-1) or approximately 11 ml min(-1) for 240 min). NaLoading did not change MAP or GFR (by clearance of (51)Cr-EDTA). Significant natriuresis occurred within 1 h (from 9 +/- 3 to 13 +/- 2 micromol 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 (NO(x)). In conclusion, sodium excretion may increase 7-fold without changes in MAP, GFR, plasma ANP, plasma oxytocin, and cGMP- and NO(x) 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. |
| Databáze: | OpenAIRE |
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