α‐ADRENOCEPTOR PROPERTIES IN RAT STRAINS SENSITIVE OR RESISTANT TO SALT‐INDUCED HYPERTENSION

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Abstract
Summary—Cerebral and renal α‐adrenoceptors are implicated in the control of sympathetic activity and of sodium reabsorption respectively. In addition, sodium ions play an important role in the regulation of either α‐adrenoceptor densities and affinities for adrenergic agonists. In the present study, α‐adrenoceptor properties were investigated in genetically predetermined salt‐sensitive and salt‐resistant Dahl and Sabra rats.Cerebral α2‐adrenoceptor densities were higher in salt‐resistant than in salt‐sensitive Dahl and Sabra rats. In contrast, renal α2‐adrenoceptor density was higher in salt‐sensitive than in salt‐resistant rats. No difference in cerebral and renal α1‐adrenoceptor densities was observed between Dahl and Sabra substrains. Noradrenaline content in cerebral and renal cortex were also similar in both these rat substrains.Sodium ions markedly increased cerebral and renal high‐affinity α2‐adrenoceptor densities in salt‐sensitive but not in salt‐resistant rats. Cerebral and renal α1‐adrenoceptor densities were unchanged in salt‐sensitive and salt‐resistant substrains of Dahl and Sabra rats. In addition, sodium ions reduced the affinity of adrenaline for renal α2‐adrenoceptors in salt‐sensitive rats but not in salt‐resistant rats.We can conclude that there exist genetically determined differences in the densities and properties of cerebral and renal α2‐adrenoceptors between salt‐sensitive and salt‐resistant rat strains. Abnormal densities of α2‐adrenoceptors may play a primary role in the role in the development of hypertension in salt‐sensitive animals. These results also suggest an association between absence of sodium regulation of α2‐adrenoceptors and resistance to salt‐induced hypertension. The absence of sodium regulation in salt‐resistant rats may be linked either to a particular receptor conformation or to an abnormal structure of the receptor system. This property may represent a genetically‐mediated change responsible for the resistance to the development of salt‐induced hypertension.