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Nitric oxide inhibition and the impact on renal nerve-mediated antinatriuresis and antidiuresis in the anaesthetized rat.
J Physiol. 2005 Dec 15; 569(Pt 3):849-56.JP

Abstract

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 microg kg(-1) min(-1)), 1400W (20 microg kg(-1) min(-1)), or S-methyl-thiocitrulline (SMTC) (20 microg 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(Na)V), 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(Na)V 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(Na)V 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(Na)V 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.

Authors+Show Affiliations

Department of Physiology, Aras Windle, University College Cork, Cork, Republic of Ireland.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16239274

Citation

Bagnall, N M., et al. "Nitric Oxide Inhibition and the Impact On Renal Nerve-mediated Antinatriuresis and Antidiuresis in the Anaesthetized Rat." The Journal of Physiology, vol. 569, no. Pt 3, 2005, pp. 849-56.
Bagnall NM, Dent PC, Walkowska A, et al. Nitric oxide inhibition and the impact on renal nerve-mediated antinatriuresis and antidiuresis in the anaesthetized rat. J Physiol. 2005;569(Pt 3):849-56.
Bagnall, N. M., Dent, P. C., Walkowska, A., Sadowski, J., & Johns, E. J. (2005). Nitric oxide inhibition and the impact on renal nerve-mediated antinatriuresis and antidiuresis in the anaesthetized rat. The Journal of Physiology, 569(Pt 3), 849-56.
Bagnall NM, et al. Nitric Oxide Inhibition and the Impact On Renal Nerve-mediated Antinatriuresis and Antidiuresis in the Anaesthetized Rat. J Physiol. 2005 Dec 15;569(Pt 3):849-56. PubMed PMID: 16239274.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitric oxide inhibition and the impact on renal nerve-mediated antinatriuresis and antidiuresis in the anaesthetized rat. AU - Bagnall,N M, AU - Dent,P C, AU - Walkowska,A, AU - Sadowski,J, AU - Johns,E J, Y1 - 2005/10/20/ PY - 2005/10/22/pubmed PY - 2006/5/5/medline PY - 2005/10/22/entrez SP - 849 EP - 56 JF - The Journal of physiology JO - J Physiol VL - 569 IS - Pt 3 N2 - 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 microg kg(-1) min(-1)), 1400W (20 microg kg(-1) min(-1)), or S-methyl-thiocitrulline (SMTC) (20 microg 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(Na)V), 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(Na)V 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(Na)V 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(Na)V 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. SN - 0022-3751 UR - https://www.unboundmedicine.com/medline/citation/16239274/Nitric_oxide_inhibition_and_the_impact_on_renal_nerve_mediated_antinatriuresis_and_antidiuresis_in_the_anaesthetized_rat_ L2 - https://doi.org/10.1113/jphysiol.2005.097709 DB - PRIME DP - Unbound Medicine ER -