This study assess the effects of glucocorticoids on dopamine excretion and
evaluates the participation of renal dopamine in the effects of glucocortic
oids on renal function and Na+ excretion. Dexamethasone (i.m.; 0.5 mg/kg) w
as administered to male Wistar rats on day 2 or on days 2 and 5. Daily urin
ary excretions of Na+, dihydroxyphenylalanine (DOPA), dopamine and dihydrox
yphenylacetic acid were determined from day 1 to day 7. Renal function was
evaluated 8 h after dexamethasone administration in a separate group. The f
irst dose of dexamethasone increased about 100% diuresis and natriuresis, i
ncreased urinary DOPA and renal plasma flow, and did not affect urinary dop
amine or the other parameters evaluated. These effects were not affected by
previous administration of haloperidol. The second dexamethasone dose incr
eased about 200% diuresis and natriuresis, increased urinary dopamine, DOPA
, dihydroxyphenylacetic acid, U-osm X V and both glomerular filtration rate
and renal plasma flow. Carbidopa administered before the second dexamethas
one dose blunted both the diuretic and the natriuretic response whereas hal
operidol abolished or blunted all the effects of the second dexamethasone d
ose. These results show that modifications in renal dopamine production pro
duced by corticoids may contribute to the effects of these hormones on Nabalance and diuresis and suggest that regardless the factor that promotes a
n increase in renal perfusion and glomerular filtration rate during long te
rm administration of glucocorticoids, a dopaminergic mechanism is actively
involved in the maintenance of these hemodynamic changes. (C) 1999 Elsevier
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