Aldosterone up-regulates mRNA for the alpha3 and beta1 isoforms of (Na,K)-ATPase in several brain regions from adrenalectomized rats.

In physiological doses, mineralocorticoids (MC) normalize the high salt intake developed after adrenalectomy. We have studied whether this effect of MC is accompanied by changes in the mRNA of neuronal alpha3 and beta1 subunits of the (Na,K)-ATPase because this enzyme could by a mediator of MC action in target cells. We employed [35S]oligonucleotide probes for the mentioned subunits hybridized to brain sections from adrenalectomized rats and adrenalectomized rats receiving aldosterone (ALDO) during 4 days. Using t-test statistics to measure differences in mean levels of grain density, and the Kolmogorov-Smirnov non-parametric test applied to frequency histograms, we showed that ALDO increased the alpha3 subunit mRNA in the septum medialis, preoptic area medialis, caudate-putamen, periventricular gray substance, amygdala lateralis, hippocampal subfields CA1 to CA4 and the gyrus dentatus. Significant increases for the beta1 subunit mRNA were found in periventricular gray substance, the CA1-CA4 hippocampal subfields and gyrus dentatus. Therefore, the salt-suppression effect of MC was accompanied by coordinate increases in (Na,K)-ATPase alpha3 and beta1 subunit mRNA in the hippocampus, gyrus dentatus and periventricular gray substance, whereas in other regions the stimulatory effect was exclusive of the alpha3 subunit mRNA only. The results suggest that the enzyme could be a target of ALDO action not only in areas related to salt appetite control (amygdala, preoptic area) but also in brain regions subserving other functions of the MC.