Sodium regulation of α2-adrenoreceptors in dahl rats : Effect of feeding a low or high salt diet

Abstract

Sodium regulation of α 2-adrenoreceptors was investigated in inbred salt-sensitive (S) and inbred salt-resistant (R) rats fed a high or low salt diet. The systolic blood pressure was higher in S rats than in R rats, and this difference was obviously greater on a high salt diet. In rats fed a low or high salt diet, S rats had higher α 2-adrenoreceptor density in the kidneys compared with R rats as measured by [ 3H]yohimbine binding and Scatchard analysis. The affinity of the receptors in the kidney for the antagonist, yohimbine, was nearly the same in these two strains either on a low or high salt diet. In the brain, the affinities or the numbers of receptors were not significantly different whether these two strains were fed a low or high salt diet. Inclusion of NaCl up to 80 mM in the assay medium did not alter the in vitro binding of [ 3H]yohimbine in the kidney or brain. On the other hand, inclusion of NaCl in the assay medium reduced the ability of epinephrine in competing with [ 3H]yohimbine for the receptor sites in the kidney and in the brain, and this effect of NaCl was the same in a given tissue between S and R rats, whether they were fed a low or high salt diet. These results suggest that: (1) in the kidneys, the receptor density and not the receptor affinity was different between S and R strains whether they were fed a low or high salt diet; (2) in the brain, the receptor density and affinity were the same between S and R rats regardless of the diet (low or high salt), indicating that the sodium salt diet modulates the peripheral but not the central α 2-adrenoreceptors; and this modulatory effect was observed only in S rats; (3) Na + was able to reduce the affinity of the agonist (epinephrine) for the receptors in both S and R rats, and this effect of Na + on central and peripheral α 2-adrenoreceptors was similar in prehypertensive rats and rats with salt-induced hypertension; and (4) the resistance of R rats to salt-induced hypertension was not due to the absence of Na + binding component involved in the regulation of α 2-adrenoreceptor-adenylate cyclase complex.