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This Article Full Text Full Text (PDF) All Versions of this Article: 294/1/R17    most recent 00435.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Kjolby, M. Articles by Bie, P. PubMed PubMed Citation Articles by Kjolby, M. Articles by Bie, P.

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Control Mechanisms of Renin Synthesis and Release: A 21st Century Perspective

Chronic activation of plasma renin is log-linearly related to dietary sodium and eliminates natriuresis in response to a pulse change in total body sodium

Department of Physiology and Pharmacology, Institute of Medical Biology, University of Southern Denmark, Odense, Denmark

Submitted 21 June 2007 ; accepted in final form 7 November 2007

Responses to acute sodium loading depend on the load and on the level of chronic sodium intake. To test the hypothesis that an acute step increase in total body sodium (TBS) elicits a natriuretic response, which is dependent on the chronic level of TBS, we measured the effects of a bolus of NaCl during different low-sodium diets spanning a 25-fold change in sodium intake on elements of the renin-angiotensin-aldosterone system (RAAS) and on natriuresis. To custom-made, low-sodium chow (0.003%), NaCl was added to provide four levels of intake, 0.03–0.75 mmol·kg^–1·day^–1 for 7 days. Acute NaCl administration increased PV (+6.3–8.9%) and plasma sodium concentration (2%) and decreased plasma protein concentration (–6.4–8.1%). Plasma ANG II and aldosterone concentrations decreased transiently. Potassium excretion increased substantially. Sodium excretion, arterial blood pressure, glomerular filtration rate, urine flow, plasma potassium, and plasma renin activity did not change. The results indicate that sodium excretion is controlled by neurohumoral mechanisms that are quite resistant to acute changes in plasma volume and colloid osmotic pressure and are not down-regulated within 2 h. With previous data, we demonstrate that RAAS variables are log-linearly related to sodium intake over a >250-fold range in sodium intake, defining dietary sodium function lines that are simple measures of the sodium sensitivity of the RAAS. The dietary function line for plasma ANG II concentration increases from theoretical zero at a daily sodium intake of 17 mmol Na/kg (intercept) with a slope of 16 pM increase per decade of decrease in dietary sodium intake.

renin-angiotensin-aldosterone system; sodium intake; potassium; renin function line; dietary function line