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This Article Full Text Full Text (PDF) All Versions of this Article: 296/2/R436    most recent 90754.2008v1 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 Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Mølstrøm, S. Articles by Bie, P. Search for Related Content PubMed PubMed Citation Articles by Mølstrøm, S. Articles by Bie, P.

WATER AND ELECTROLYTE HOMEOSTASIS

Normotensive sodium loading in normal man: regulation of renin secretion during β-receptor blockade

¹Department of Physiology and Pharmacology, Institute of Medical Biology, University of Southern Denmark; ²Department of Anesthesiology and Intensive Care, Odense University Hospital; and ³Department of Nuclear Medicine, Odense University Hospital, Odense, Denmark

Submitted 8 September 2008 ; accepted in final form 1 December 2008

Saline administration may change renin-angiotensin-aldosterone system (RAAS) activity and sodium excretion at constant mean arterial pressure (MAP). We hypothesized that such responses are elicited mainly by renal sympathetic nerve activity by β₁-receptors (β₁-RSNA), and tested the hypothesis by studying RAAS and renal excretion during slow saline loading at constant plasma sodium concentration (Na⁺ loading; 12 µmol Na⁺·kg^–1·min^–1 for 4 h). Normal subjects were studied on low-sodium intake with and without β₁-adrenergic blockade by metoprolol. Metoprolol per se reduced RAAS activity as expected. Na⁺ loading decreased plasma renin concentration (PRC) by one-third, plasma ANG II by one-half, and plasma aldosterone by two-thirds (all P < 0.05); surprisingly, these changes were found without, as well as during, acute metoprolol administration. Concomitantly, sodium excretion increased indistinguishably with and without metoprolol (16 ± 2 to 71 ± 14 µmol/min; 13 ± 2 to 55 ± 13 µmol/min, respectively). Na⁺ loading did not increase plasma atrial natriuretic peptide, glomerular filtration rate (GFR by ⁵¹Cr-EDTA), MAP, or cardiac output (CO by impedance cardiography), but increased central venous pressure (CVP) by 2.0 mmHg (P < 0.05). During Na⁺ loading, sodium excretion increased with CVP at an average slope of 7 µmol·min^–1·mmHg^–1. Concomitantly, plasma vasopressin decreased by 30–40% (P < 0.05). In conclusion, β₁-adrenoceptor blockade affects neither the acute saline-mediated deactivation of RAAS nor the associated natriuretic response, and the RAAS response to modest saline loading seems independent of changes in MAP, CO, GFR, β₁-mediated effects of norepinephrine, and ANP. Unexpectedly, the results do not allow assessment of the relative importance of RAAS-dependent and -independent regulation of renal sodium excretion. The results are compatible with the notion that at constant arterial pressure, a volume receptor elicited reduction in RSNA via receptors other than β₁-adrenoceptors, decreases renal tubular sodium reabsorption proximal to the macula densa leading to increased NaCl concentration at the macula densa, and subsequent inhibition of renin secretion.

blood pressure; angiotensin; aldosterone; natriuresis; sodium balance