Regulation of renal alpha 2-adrenoceptor activity in Dahl salt-sensitive rats by dietary sodium changes

The objective of the study was to evaluate the concept that genetically predisposed salt-sensitivity contributes to an increased adrenergic susceptibility and renal alpha 2-adrenoceptor (A2) abnormality in Dahl salt-sensitive hypertensive rats. The results showed: i) After 2 months of Na-loading (8% NaCl) Dahl salt-sensitive (DSS) rats expressed increased sodium and water retention which paralleled gradual development of diastolic hypertension. Low Na diet (0.5% NaCl) does not prevent hypertension but delays its development. ii) The increased activity of the sympathetic nervous system (SNS), in DSS rats corresponded to the development of hypertension and was stimulated by Na-loading. It was assessed by plasma catecholamine levels and heart rate changes. iii) The increased density of renal A2 by 29% was upregulated by high sodium diet, and coupled with increased norepinephrine level by 53%, only in DSS but not in DSR rats. iv) No strain renal A2 and epinephrine differences between DSS and DSR were found in weanling, prehypertensive rats, or in the adult DSS and DSR on low Na diet. By mediating an enhanced receptor-coupled response, such as increased proximal tubular sodium reabsorption during sodium loading, a genetic abnormality of renal alpha 2-adrenoceptors may contribute to some of the pathophysiologic derangements leading to hypertension in Dahl salt-sensitive rats.