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This Article Full Text Full Text (PDF) All Versions of this Article: 559/3/939    most recent jphysiol.2004.066670v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Seeliger, E. Articles by Reinhardt, H. W. Search for Related Content PubMed PubMed Citation Articles by Seeliger, E. Articles by Reinhardt, H. W.

¹ Institute of Physiology, University Clinics Charité, Berlin, Germany
² Department of Medical Physiology, University of Copenhagen, Copenhagen, Denmark
³ Institute of Medical Biology, University of Southern Denmark, Odense, Denmark

The study was designed to determine to what extent moderate elevation of renal perfusion pressure (RPP) via the mechanism of ‘pressure natriuresis’ contributes to the natriuresis induced by acute I.V. saline loading. Nine Beagle dogs maintained on ample sodium intake (5.5 mmol (kg body mass)^–1 day^–1) were chronically equipped with an aortic occluder to servocontrol RPP, a bladder catheter to measure renal function, and catheters for measurement of RPP and mean arterial blood pressure (MABP). A swivel system allowed free movement in the kennel during experiments. Isotonic saline loading (500 ml in 100 min) was studied as follows: with and without servocontrol of RPP, and these two protocols repeated in the presence of angiotensin-converting enzyme inhibition (ACEI, Enalapril, 2 mg (kg body mass)^–1). Saline loading increased MABP by about 12 mmHg and sodium excretion from about 28 µmol min^–1 up to about 350 µmol min^–1. Without ACEI, servocontrol of RPP at 10% below control 24 h MABP slightly delayed the onset of the saline-induced natriuresis, but did not reduce peak sodium excretion or cumulative sodium excretion. The slight delay most probably resulted from pressure-controlled renin release because, with ACEI, servocontrol of RPP did not delay or reduce the saline-induced natriuresis. In conclusion, pressure natriuresis does not contribute to the natriuresis following acute saline loading.

(Received 28 April 2004; accepted after revision 13 July 2004; first published online 14 July 2004)
Corresponding author E. Seeliger: Institut für Physiologie, Charité Universitätsmedizin Berlin, Tucholskystr. 2, Berlin 10177, Germany. Email: erdmann.seeliger{at}charite.de

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