CHANGES IN CENTRAL ALPHA-ADRENOCEPTORS AND NORADRENALINE CONTENT AFTER HIGH SODIUM-INTAKE IN SABRA SALT-SENSITIVE AND SALT-RESISTANT RATS

Several studies have suggested a correlation between sodium accumulation and the development of hypertension. However, the mechanisms whereby sodium is able to increase blood pressure remain unclear. In the present study, .alpha.-adrenoceptors and noradrenaline contents have been studied in the cerebral cortex, hypothalamus and medulla oblongata in the Sabra rat strain in order to define their role in the resistance or sensitivity to sodium-induced hypertension. .alpha.-Adrenoceptors were defined using the selective ligands 3H-prazosin and 3H-rauwolscine for .alpha.1- and .alpha.2-adrenoceptors, respectively. Under normal sodium diet, .alpha.2-adrenoceptor density was higher in cerebral cortex and lower in hypothalamus and medulla oblongata of SBN (salt-resistant) compared to SBH (salt-sensitive) rats. Five weeks of high sodium intake induced a decrease in .alpha.2-adrenoceptor density in cerebral cortex and an increase in hypothalamus only in SBN rats. These changes abolished the differences between SBH and SBN rats observed with a normal sodium diet. No changes in density and affinity of .alpha.2-adrenoceptors were observed in medulla oblongata of SBN and SBH rats. Density and affinity of .alpha.a-adrenoceptors were similar in SBN and SBH rats in all the tissues studied and they were unaffected by the high sodium diet. Noradrenaline contents in cerebral cortex, hypothalamus and medulla oblongata were also similar in the two rat substrains under normal sodium diet, but high sodium intake induced a decrease cerebrocortical noradrenaline content only in SBN rats. These results lead to the following conclusions: (i) changes in noradrenaline content in cerebral cortex and in .alpha.2-adrenoceptor density in both cerebral cortex and hypothalamus might serve to maintain a normal sympathetic activity on blood pressure in SBN after high sodium intake, (ii) the .alpha.2-adrenoceptor density in both cerebral cortex and hypothalamus might serve to maintain a normal sympathetic activity and blood pressure in SBN after high sodium intake, (ii) the .alpha.2-adrenoceptor abnormality in the medulla oblongata, not dependent on sodium intake, might be responsible for the higher blood pressure in SBH than in SBN untreated rats, (iii) the adrenergic nervous system is probably involved in sodium induced hypertension.