HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 569/3/849    most recent jphysiol.2005.097709v1 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 Bagnall, N. M. Articles by Johns, E. J. Search for Related Content PubMed PubMed Citation Articles by Bagnall, N. M. Articles by Johns, E. J.

¹ Department of Physiology, University College Cork, Cork, Republic of Ireland
² Laboratory of Renal and Body Fluid Physiology, M. Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland

The contribution of nitric oxide (NO) to the antinatriuresis and antidiuresis caused by low-level electrical stimulation of the renal sympathetic nerves (RNS) was investigated in rats anaesthetized with chloralose–urethane. Groups of rats, n= 6, were given I.V. infusions of vehicle, L-NAME (10 µg kg^–1 min^–1), 1400W (20 µg kg^–1 min^–1), or S-methyl-thiocitrulline (SMTC) (20 µg kg^–1 min^–1) to inhibit NO synthesis non-selectively or selectively to block the inducible or neuronal NOS isoforms (iNOS and nNOS, respectively). Following baseline measurements of blood pressure (BP), renal blood flow (RBF), glomerular filtration rate (GFR), urine flow (UV) and sodium excretion (U_NaV), RNS was performed at 15 V, 2 ms duration with a frequency between 0.5 and 1.0 Hz. RNS did not cause measurable changes in BP, RBF or GFR in any of the groups. In untreated rats, RNS decreased UV and U_NaV by 40–50% (both P < 0.01), but these excretory responses were prevented in L-NAME-treated rats. In the presence of 1400W I.V., RNS caused reversible reductions in both UV and U_NaV of 40–50% (both P < 0.01), while in SMTC-treated rats, RNS caused an inconsistent fall in UV, but a significant reduction (P < 0.05) in U_NaV of 21%. These data demonstrated that the renal nerve-mediated antinatriuresis and antidiuresis was dependent on the presence of NO, generated in part by nNOS. The findings suggest that NO importantly modulates the neural control of fluid reabsorption; the control may be facilitatory at a presynaptic level but inhibitory on tubular reabsorptive processes.

(Received 29 August 2005; accepted after revision 18 October 2005; first published online 20 October 2005)
Corresponding author E. J. Johns: Department of Physiology, Aras Windle, University College Cork, Cork, Republic of Ireland. Email: e.j.johns{at}ucc.ie

This article has been cited by other articles:

				L. M. Yamaleyeva, P. E. Gallagher, S. Vinsant, and M. C. Chappell Discoordinate regulation of renal nitric oxide synthase isoforms in ovariectomized mRen2.Lewis rats Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2007; 292(2): R819 - R826. [Abstract] [Full Text] [PDF]