title: Nitric oxide inhibition and the impact on renal nerve-mediated antinatriuresis and antidiuresis in the anaesthetized rat.
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.affiliation: Department of Physiology, Aras Windle, University College Cork, Cork, Republic of Ireland.
authors.forename: N M
authors.initials: NM
authors.lastname: Bagnall
authors.forename: P C
authors.initials: PC
authors.lastname: Dent
authors.forename: A
authors.initials: A
authors.lastname: Walkowska
authors.forename: J
authors.initials: J
authors.lastname: Sadowski
authors.forename: E J
authors.initials: EJ
authors.lastname: Johns
mesh_terms: D000578:Amidines / Q000494:pharmacology; D000758:Anesthesia; D000818:Animals; D001596:Benzylamines / Q000494:pharmacology; D002956:Citrulline / Q000031:analogs & derivatives / Q000494:pharmacology; D004231:Diuresis / Q000187:drug effects*; D004558:Electric Stimulation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007262:Infusions, Intravenous; D007668:Kidney / Q000294:innervation* / Q000502:physiology; D008297:Male; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009318:Natriuresis / Q000187:drug effects*; D009451:Neuroeffector Junction / Q000187:drug effects / Q000201:enzymology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors; D051381:Rats; D017208:Rats, Wistar; D013564:Sympathetic Nervous System / Q000187:drug effects / Q000201:enzymology*; D013890:Thiourea / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D000578:Amidines; D001596:Benzylamines; D004791:Enzyme Inhibitors; C104820:N-(3-(aminomethyl)benzyl)acetamidine; D002956:Citrulline; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; D052247:Nitric Oxide Synthase Type II; C496322:Nos1 protein, rat; C496318:Nos2 protein, rat; D013890:Thiourea; C086717:S-methylthiocitrulline; D019331:NG-Nitroarginine Methyl Ester