Central administration of zinc increases renal sodium and potassium excretion in rats

The aim of the present study was to investigate the effect of acute third v entricle injections of zinc on the brain control of renal sodium and potass ium excretion. Adult Wistar male rats received third ventricle injections o f zinc acetate in three different doses (0.03, 0.3 and 3.0 nmol/rat). Third ventricle administration of zinc acetate provoked a significant intensific ation of natriuresis and kaliuresis as compared to sodium acetate-treated c ontrols. When rats were pretreated with losartan, a selective angiotensin I I AT, receptor antagonist (10.8 nmol/rat into the third ventricle 10 min be fore central zinc injection) the increase in both natriuresis and kaliuresi s was abolished. Furthermore, pretreatment with gadolinium, a calcium chann el blocker (0.3 nmol/rat into the third ventricle 20 min before central zin c injection), also blunted the increase in renal sodium and potassium excre tion seen in animals receiving zinc alone. In a group of rats receiving the same water load used in the previous experiments, the injection of zinc ac etate into the third ventricle (3.0 nmol/rat) did not modify arterial blood pressure. It is suggested that zinc in the central nervous system may be i nvolved in the control of renal sodium and potassium excretion by a mechani sm unrelated to blood pressure increase. It is also shown that both natriur etic and kaliuretic actions of zinc depend on AT, receptor activation. What ever should be the mechanism(s) related to the central effects of zinc here evidenced, the functional integrity of calcium channels is required. (C) 1 999 Elsevier Science B.V. All rights reserved.