Previous studies carried out in our laboratories demonstrated that dietary NaCl supplementation induced an increase in blood pressure associated with a reduction in noradrenaline release in the anterior hypothalamic region of NaCl-sensitive spontaneously hypertensive rats (SHR). The present study tested the hypothesis that this reduction in noradrenaline release induces a compensatory increase in α2-adrenoceptor number in the anterior hypothalamic region of SHR. Low affinity p-[3H]aminoclonidine (α2-adrenoceptor agonist) binding in the anterior hypothalamic region was increased significantly in SHR, but not in normotensive Wistar-Kyoto (WKY) rats on a high (compared to a basal) NaCl diet. Increased p-[3H]aminoclonidine binding was present at 1 and 2 weeks following initiation of the diets. In contrast, in the posterior hypothalamic region of SHR, α2-adrenoceptors were significantly reduced following 1 week on the high (compared to basal) NaCl diet, and no difference between groups was observed following 2 weeks on the diets. The high NaCl diet did not alter α2-adrenoceptors in the medulla, nor did it affect α1- or β-adrenoceptors in any brain region studied in either SHR or WKY. In SHR, dietary Ca2+ supplementation diminished the blood pressure elevation associated with high NaCl diets, and simultaneously prevented the NaCl induced increase in α2-adrenoceptors in the anterior hypothalamic region. These data support the hypothesis that, in susceptible individuals, changes in noradrenergic transmission in the anterior hypothalamic region contribute to the cardiovascular effects of dietary NaCl loading and Ca2+ supplementation. © 1988.
