Klangkalya B, Sripairojthikoon W, Oparil S, Wyss J M
Department of Cell Biology, University of Alabama, Birmingham 35294.
Brain Res. 1988 Jun 7;451(1-2):77-84. doi: 10.1016/0006-8993(88)90751-2.
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 alpha 2-adrenoceptor number in the anterior hypothalamic region of SHR. Low affinity p-[3H]aminoclonidine (alpha 2-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, alpha 2-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 alpha 2-adrenoceptors in the medulla, nor did it affect alpha 1- or beta-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 alpha 2-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.
我们实验室之前开展的研究表明，对盐敏感的自发性高血压大鼠（SHR）补充膳食氯化钠会导致血压升高，同时下丘脑前部去甲肾上腺素释放减少。本研究检验了这样一个假设，即去甲肾上腺素释放的减少会导致SHR下丘脑前部α2 -肾上腺素能受体数量代偿性增加。在高盐（与基础盐摄入相比）饮食条件下，SHR下丘脑前部低亲和力的对-[3H]氨基可乐定（α2 -肾上腺素能受体激动剂）结合显著增加，但正常血压的Wistar - Kyoto（WKY）大鼠没有这种情况。在开始饮食后的1周和2周时均出现了对-[3H]氨基可乐定结合增加的情况。相比之下，在SHR下丘脑后部，高盐（与基础盐摄入相比）饮食1周后α2 -肾上腺素能受体显著减少，饮食2周后各实验组之间未观察到差异。高盐饮食并未改变延髓中的α2 -肾上腺素能受体，对SHR或WKY任何研究脑区中的α1 -或β -肾上腺素能受体也没有影响。在SHR中，补充膳食钙可减轻与高盐饮食相关的血压升高，同时防止高盐诱导的下丘脑前部α2 -肾上腺素能受体增加。这些数据支持了这样一个假设，即在易感个体中，下丘脑前部去甲肾上腺素能传递的变化促成了膳食氯化钠摄入和补钙对心血管系统的影响。
