Low sodium intake induces an increase in renal Monoamine Oxidase (MAO) activity in the rat. Involvement of an Angiotensin II dependent mechanism.

DE LUCA SAROBE, VERÓNICA; CARRANZA, ANDREA; LEVIN GLORIA; BARONTINI, MARTA; ARRIZURIETA, ELVIRA E; IBARRA, FERNANDO

St. Louis - Missouri - USA

Congreso; Renal Week 2004; 2004

American Society of Nephrology

Dopamine and Angiotensin II play opposite actions on renal function. We tested here whether Angiotensin II is able to enhance renal dopamine breakdown by stimulating monoaminoxidase in the kidney. Rats received normal salt (NS) or low salt diet (LS) for five days with or without the addition of Losartan in the drinking water (20 mg kg-1bwt d-1). Monoaminoxidase activity was higher in cortical homogenates of LS rats as compared with NS (in nmol mg tissue-1 hr-1  9.82±0.59 vs 7.66±0.52, p<0.05). Urinary dopamine was lower in LS than in NS rats (543±32 vs 680±34ng d-1 100g-1bwt, p <0.05), while 3,4-dihydroxyphenilacetic acid (DOPAC) excretion and DOPAC/dopamine ratio both showed a trend to be higher in LS group. Under Losartan a significant decrease in monoaminoxidase activity was observed in cortical homogenates from LS+Los rats (7.34±0.49 nmol mg tissue-1 hr-1, p<0.01, vs LS), while the significant difference in urinary dopamine between NS and LS rats disappeared and urinary DOPAC and DOPAC/dopamine ratio fell significantly in LS+Los group as compared with LS (3081±681 vs 1199±328 ng d-1 100g-1 bwt and 5.1±1.2 vs 1.90±0.5, respectively, both p<0.01). Losartan increased urinary volume and sodium excretion only in LS+Los group. Losartan did not cause changes in NS+Los group. We conclude that low levels of dopamine in the urine of LS rats are at least partially due to an increase in the activity of renal monoaminoxidase, and that Angiotensin II mediates this increase through stimulation of AT1 receptors. This mechanism could alter dopamine metabolism in those conditions which course with elevated Angiotensin II.