title: Role of nitric oxide in the control of renal oxygen consumption and the regulation of chemical work in the kidney.
abstract: Inhibition of NO synthesis has recently been shown to increase oxygen extraction in vivo, and NO has been proposed to play a significant role in the regulation of oxygen consumption by both skeletal and cardiac muscle in vivo and in vitro. It was our aim to determine whether NO also has such a role in the kidney, a tissue with a relatively low basal oxygen extraction. In chronically instrumented conscious dogs, administration of an inhibitor of NO synthase, nitro-L-arginine (NLA, 30 mg/kg i.v.), caused a maintained increase in mean arterial pressure and renal vascular resistance and a decrease in heart rate (all P<0.05). At 60 minutes, urine flow rate and glomerular flow rate decreased by 44+/-12% and 45+/-7%, respectively; moreover, the amount of sodium reabsorbed fell from 16+/-1.7 to 8.5+/-1.1 mmol/min (all P<0.05). At this time, oxygen uptake and extraction increased markedly by 115+/-37% and 102+/-34%, respectively (P<0.05). Oxygen consumption also significantly increased from 4.5+/-0.6 to 7.1+/-0.9 mL O2/min. Most important, the ratio of oxygen consumption to sodium reabsorbed increased dramatically from 0.33+/-0.07 to 0.75+/-0.11 mL O2/mmol Na+ (P<0.05), suggesting a reduction in renal efficiency for transporting sodium. In vitro, both a NO-donating agent and the NO synthase-stimulating agonist bradykinin significantly decreased both cortical and medullary renal oxygen consumption. In conclusion, NO plays a role in maintaining a balance between oxygen consumption and sodium reabsorption, the major ATP-consuming process in the kidney, in conscious dogs, and NO can inhibit mitochondrial oxygen consumption in canine renal slices in vitro.
authors.affiliation: Department of Physiology, New York Medical College, Valhalla 10595, USA.
authors.forename: S K
authors.initials: SK
authors.lastname: Laycock
authors.forename: T
authors.initials: T
authors.lastname: Vogel
authors.forename: P R
authors.initials: PR
authors.lastname: Forfia
authors.forename: J
authors.initials: J
authors.lastname: Tuzman
authors.forename: X
authors.initials: X
authors.lastname: Xu
authors.forename: M
authors.initials: M
authors.lastname: Ochoa
authors.forename: C I
authors.initials: CI
authors.lastname: Thompson
authors.forename: A
authors.initials: A
authors.lastname: Nasjletti
authors.forename: T H
authors.initials: TH
authors.lastname: Hintze
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000187:drug effects; D004285:Dogs; D004734:Energy Metabolism; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005919:Glomerular Filtration Rate / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000502:physiology*; D007677:Kidney Function Tests; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000494:pharmacology; D010101:Oxygen Consumption; D012964:Sodium / Q000378:metabolism; D014655:Vascular Resistance / Q000187:drug effects
chemical_list: D004791:Enzyme Inhibitors; D019335:Nitroarginine; D009569:Nitric Oxide; D012964:Sodium; D019001:Nitric Oxide Synthase