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This Article Full Text Full Text (PDF) All Versions of this Article: 294/4/R1130    most recent 00908.2007v1 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 Web of Science 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 Web of Science (2) Citing Articles via Google Scholar Google Scholar Articles by Kompanowska-Jezierska, E. Articles by Bie, P. Search for Related Content PubMed PubMed Citation Articles by Kompanowska-Jezierska, E. Articles by Bie, P.

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

Renal nerves and nNOS: roles in natriuresis of acute isovolumetric sodium loading in conscious rats

Elbieta Kompanowska-Jezierska,² Helle Wolff,¹ Marta Kuczeriszka,² Jan B. Gramsbergen,³ Agnieszka Walkowska,² Edward J. Johns,⁴ and Peter Bie¹

¹Department of Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark; ²Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre of the Polish Academy of Sciences, Warsaw, Poland; ³Department of Anatomy and Neurobiology, University of Southern Denmark, Odense, Denmark; and ⁴Department of Physiology, University College Cork, Cork, Republic of Ireland

Submitted 20 December 2007 ; accepted in final form 21 January 2008

It was hypothesized that renal sympathetic nerve activity (RSNA) and neuronal nitric oxide synthase (nNOS) are involved in the acute inhibition of renin secretion and the natriuresis following slow NaCl loading (NaLoad) and that RSNA participates in the regulation of arterial blood pressure (MABP). This was tested by NaLoad after chronic renal denervation with and without inhibition of nNOS by S-methyl-thiocitrulline (SMTC). In addition, the acute effects of renal denervation on MABP and sodium balance were assessed. Rats were investigated in the conscious, catheterized state, in metabolic cages, and acutely during anesthesia. NaLoad was performed over 2 h by intravenous infusion of hypertonic solution (50 µmol·min^–1·kg body mass^–1) at constant body volume conditions. SMTC was coinfused in amounts (20 µg·min^–1·kg^–1) reported to selectively inhibit nNOS. Directly measured MABPs of acutely and chronically denervated rats were less than control (15% and 9%, respectively, P < 0.005). Plasma renin concentration (PRC) was reduced by renal denervation (14.5 ± 0.2 vs. 19.3 ± 1.3 mIU/l, P < 0.005) and by nNOS inhibition (12.4 ± 2.3 vs. 19.6 ± 1.6 mlU/l, P < 0.005). NaLoad reduced PRC (P < 0.05) and elevated MABP modestly (P < 0.05) and increased sodium excretion six-fold, irrespective of renal denervation and SMTC. The metabolic data demonstrated that renal denervation lowered sodium balance during the first days after denervation (P < 0.001). These data show that renal denervation decreases MABP and renin secretion. However, neither renal denervation nor nNOS inhibition affects either the renin down-regulation or the natriuretic response to acute sodium loading. Acute sodium-driven renin regulation seems independent of RSNA and nNOS under the present conditions.

plasma renin concentration; total body sodium; blood pressure; sodium excretion

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