title: Low-dose nitric oxide inhibition produces a negative sodium balance in conscious dogs.
abstract: Nitric oxide modulates renal hemodynamics and salt and water handling. Studies on the latter have provided conflicting results, however. Electrolyte and water balances were therefore studied in 28 beagles for 4 d, to determine the various effects of nitric oxide synthase (NOS) inhibition on renal function. The dogs were chronically equipped with aortic occluders to reduce renal perfusion pressure (RPP), bladder catheters, and catheters for measurements of RPP and mean arterial BP. A swivel system allowed free movement within the kennels. In a first set of experiments, a nonpressor dose of L-Nomega-nitroarginine (LN) (3 microg/min per kg body wt) was administered, to prevent increases in mean arterial BP and thus pressure effects on renin release and natriuresis. Remarkably, the nonpressor dose of LN caused a negative sodium balance. The natriuretic effect may involve reduced plasma renin activity, reduced aldosterone concentrations, and increased atrial natriuretic peptide concentrations. Changes in aldosterone levels, however, were the only parameters to parallel the time course of sodium excretion. In a second set of experiments, a sodium-retaining challenge was elicited by reduction of RPP. Dogs without NOS inhibition escaped sodium retention during RPP reduction after 2 d ("pressure escape"). LN neither ameliorated nor aggravated the sodium-retaining effect of reduced RPP, nor did it compromise the accomplishment of pressure escape. In conclusion, inhibition of NOS with a low dose of LN results in a reduction of total-body sodium. This effect mainly relies on reduced aldosterone concentrations. Furthermore, LN does not change the regulatory response to long-term RPP reduction.
authors.affiliation: Johannes Müller Institute for Physiology, Campus Charité Mitte, Humboldt University of Berlin, Berlin, Germany.
authors.forename: Erdmann
authors.initials: E
authors.lastname: Seeliger
authors.affiliation: Johannes Müller Institute for Physiology, Campus Charité Mitte, Humboldt University of Berlin, Berlin, Germany.
authors.forename: Pontus B
authors.initials: PB
authors.lastname: Persson
authors.affiliation: Experimentelle Anaesthesie, Campus Virchow Klinikum, Humboldt University of Berlin, Berlin, Germany.
authors.forename: Willehad
authors.initials: W
authors.lastname: Boemke
authors.affiliation: Johannes Müller Institute for Physiology, Campus Charité Mitte, Humboldt University of Berlin, Berlin, Germany.
authors.forename: Götz
authors.initials: G
authors.lastname: Mollenhauer
authors.affiliation: Johannes Müller Institute for Physiology, Campus Charité Mitte, Humboldt University of Berlin, Berlin, Germany.
authors.forename: Benno
authors.initials: B
authors.lastname: Nafz
authors.affiliation: Johannes Müller Institute for Physiology, Campus Charité Mitte, Humboldt University of Berlin, Berlin, Germany.
authors.forename: H Wolfgang
authors.initials: HW
authors.lastname: Reinhardt
mesh_terms: D000450:Aldosterone / Q000378:metabolism; D000704:Analysis of Variance; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects; D001834:Body Water / Q000378:metabolism; D004285:Dogs; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics; D007668:Kidney / Q000378:metabolism* / Q000502:physiology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors* / Q000378:metabolism; D019335:Nitroarginine / Q000494:pharmacology*; D010477:Perfusion; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism*
chemical_list: D019335:Nitroarginine; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012964:Sodium; D019001:Nitric Oxide Synthase; D011188:Potassium