title: Role of nitric oxide in the reflex diuresis in rabbits during pulmonary lymphatic obstruction.
abstract: The role of nitric oxide in the reflex diuresis in response to pulmonary lymphatic drainage was examined in anaesthetized, artificially ventilated New Zealand White rabbits. Pulmonary lymphatic drainage was obstructed by raising the pressure in a pouch created from the right external jugular vein. Pulmonary lymphatic obstruction resulted in a significant increase in urine flow from an initial control value of 8.9 +/- 0.5 ml (10 min)(-1) to 12.1 +/- 0.6 ml (10 min)(-1) during lymphatic obstruction (mean +/-s.e.m.; n= 17, P < 0.001). This increase in urine flow was accompanied by a significant increase in the excretion of sodium. Additionally, renal blood flow remained unchanged during the increase in urine flow caused by lymphatic obstruction. Intravenous infusion of L-NAME, a non-selective inhibitor of nitric oxide synthase (NOS), abolished the reflex diuresis. Furthermore, intraperitoneal administration of the relatively selective neuronal NOS blocker, 7-nitroindazole also abolished the response. It was observed that infusion of a more soluble neuronal NOS blocker, 7-nitroindazole sodium salt (7-NINA), into the renal medulla also abolished the reflex diuresis. These findings suggest that the increase in urine flow in rabbits caused by pulmonary lymphatic obstruction is dependent upon the integrity of neuronal NOS activity within the renal medulla.
authors.affiliation: Division of Cardiovascular Medicine, University of California, Davis 95616, USA
authors.forename: K M
authors.initials: KM
authors.lastname: McCormick
authors.forename: S
authors.initials: S
authors.lastname: Gunawardena
authors.forename: K
authors.initials: K
authors.lastname: Ravi
authors.forename: E M
authors.initials: EM
authors.lastname: Bravo
authors.forename: C T
authors.initials: CT
authors.lastname: Kappagoda
mesh_terms: D000818:Animals; D004231:Diuresis / Q000187:drug effects / Q000502:physiology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D007191:Indazoles / Q000494:pharmacology; D007275:Injections, Intravenous; D007679:Kidney Medulla / Q000098:blood supply / Q000187:drug effects / Q000502:physiology; D008168:Lung / Q000502:physiology*; D008208:Lymphatic System / Q000503:physiopathology*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D052248:Nitric Oxide Synthase Type I; D011817:Rabbits; D012018:Reflex / Q000502:physiology*; D012079:Renal Circulation / Q000502:physiology; D014556:Urine
chemical_list: D004791:Enzyme Inhibitors; D007191:Indazoles; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D052248:Nitric Oxide Synthase Type I; C080122:7-nitroindazole; D019331:NG-Nitroarginine Methyl Ester