We studied the acute effects of cadmium third ventricle injections on
renal excretion of water, sodium and potassium in rats previously subm
itted to an oral water load equivalent to 10% of their body weight. In
jections of cadmium chloride (0.03, 0.3, and 3.0 nmol/rat) significant
ly increased sodium and potassium renal excretion without changing uri
ne flow. Pretreatment with losartan, an angiotensin II AT1 receptor an
tagonist (10.8 nmol/rat into the third ventricle 10 min before central
cadmium administration) inhibits the natriuretic effect of this metal
, being unable to reverse its kaliuretic effect. Pretreatment with gad
olinium, a calcium-channel blocker (0.3 nmol/rat into the third ventri
cle 20 min before central cadmium administration) abolishes both the n
atriuretic and the kaliuretic response of cadmium. The data clearly sh
ow that cadmium injections into the third ventricle disturb central re
gulation of renal function leading to an increased renal loss of sodiu
m and potassium. It is also evident that the natriuretic action of the
metal depends on an increase in brain angiotensin II release. Also, t
he functional integrity of calcium channels is required for the expres
sion of both the natriuretic and the kaliuretic effects of the metal.
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