title: Low sodium intake induces an increase in renal monoamine oxidase activity in the rat. Involvement of an angiotensin II dependent mechanism.
abstract: OBJECTIVE
  The interplay between natriuretic dopamine and antinatriuretic angiotensin II represents an important mechanism for the regulation of renal sodium and water excretion. Monoamine oxidase is the main metabolizing pathway for dopamine in the renal cortex. In this study, we have analysed the effect of low sodium feeding and AT1 receptor blockade on renal dopamine metabolism by monoamine oxidase.
  
  
  METHODS
  Four groups of rats were studied: 1, normal salt diet (NS); 2, low salt diet (LS); 3, NS receiving Losartan (Los, specific AT1 receptor antagonist, 20 mg kg(-1) bwt day(-1), NS + Los); 4, LS receiving Los (LS + Los).
  
  
  RESULTS
  Urinary dopamine excretion was lower in LS than in NS rats (543 +/- 32 vs. 680 +/- 34 ng day(-1) 100 g(-1) bwt, P < 0.05). When treated with Los, DOPAC excretion and urinary DOPAC/dopamine ratio fell significantly in the LS + Los group as compared with the LS group (1199 +/- 328 vs. 3081 +/- 681 ng day(-1) 100 g(-1) bwt and 1.90 +/- 0.5 vs. 5.7 +/- 1.2, respectively, both P < 0.02). Losartan increased hydroelectrolyte excretion in the LS group. No changes were found in the NS + Los group. Aromatic L-amino acid decarboxylase activity in cortex was similar in NS and LS rats. Instead, monoamine oxidase activity was higher in cortical homogenates from LS rats (in nmol mg tissue(-1) h(-1): NS 7.66 +/- 0.52; LS 9.82 +/- 0.59, P < 0.05) and this difference was abolished in LS + Los rats (7.34 +/- 0.49 nmol mg tissue(-1) h(-1), P < 0.01, vs. LS).
  
  
  CONCLUSIONS
  We have concluded that low levels of dopamine in the urine of LS rats are because of an increase in the activity of renal monoamine oxidase and that angiotensin II mediates this increase through stimulation of AT1 receptors.
authors.affiliation: Instituto de Investigaciones Médicas A. Lanari, University of Buenos Aires, Buenos Aires, Argentina.
authors.forename: V
authors.initials: V
authors.lastname: De Luca Sarobe
authors.forename: S
authors.initials: S
authors.lastname: Nowicki
authors.forename: A
authors.initials: A
authors.lastname: Carranza
authors.forename: G
authors.initials: G
authors.lastname: Levin
authors.forename: M
authors.initials: M
authors.lastname: Barontini
authors.forename: E
authors.initials: E
authors.lastname: Arrizurieta
authors.forename: F R
authors.initials: FR
authors.lastname: Ibarra
mesh_terms: D015102:3,4-Dihydroxyphenylacetic Acid / Q000652:urine; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000378:metabolism*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D004039:Diet, Sodium-Restricted / Q000379:methods*; D004298:Dopamine / Q000652:urine; D005919:Glomerular Filtration Rate / Q000502:physiology; D007668:Kidney / Q000201:enzymology*; D019808:Losartan / Q000494:pharmacology; D008297:Male; D008995:Monoamine Oxidase / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000652:urine
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D015102:3,4-Dihydroxyphenylacetic Acid; D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D008995:Monoamine Oxidase; D019808:Losartan; D004298:Dopamine