We have previously shown that sodium restriction upregulates the genes encoding angiotensin II receptor (AT1) subtypes, AT1A and AT1B, in the adrenal gland and that this upregulation is mediated by activation of the AT1 receptor. There are multiple interactions between the renin-angiotensin and the adrenergic nervous systems; thus, we conducted the present experiment to investigate whether low sodium-induced upregulation of adrenal AT1A and AT1B is modulated by the alpha1-adrenoreceptor. Seven-week-old male Wistar rats were divided into four groups and given normal sodium diet (0.5%, NS), NS+prazosin (3.5 microg x kg(-1) x min(-1) by osmotic pump), low sodium diet (0.07%, LS), or LS+prazosin. Body weight and mean arterial pressure were not modified over the 2 weeks of treatment (P>.05). Pressor responses to bolus injection of the alpha1-agonist phenylephrine were inhibited in both prazosin groups, compared with NS and LS rats (P<.05). Adrenal AT1A mRNA, determined by Northern blot analysis, was increased in LS (P<.05) but not in NS+prazosin (P>.05), compared with NS. Prazosin enhanced the LS-induced increase of AT1A mRNA (P<.05). Adrenal AT1B mRNA was increased in both LS and NS+prasozin rats, compared with NS rats (P<.05). Prazosin also enhanced the LS-induced increase in AT1B mRNA (P<.05). Therefore, blockade of alpha1-adrenoreceptor results in an enhancement of LS-induced upregulation of adrenal mRNA for AT1A and AT1B. These data suggest that the sympathetic nervous system exerts an inhibitory action, via activation of the alpha1-adrenoreceptor, on AT1A and AT1B gene expression in the adrenal gland during sodium depletion.