Diop L, Parini A, Dausse J P, Ben-Ishay D
J Hypertens Suppl. 1984 Dec;2(3):S163-5.
Cerebral and renal alpha 2-adrenoceptors, modulated in vitro by sodium ions, are implicated in the control of sympathetic activity and of sodium reabsorption, respectively. The aim of the present study was to investigate the effect of high (8%) versus normal (0.2%) sodium diet on cerebral and renal alpha-adrenoceptors of Sabra hypertensive (SBH) and normotensive (SBN) rats. After two or five weeks of high sodium diet alpha 2-adrenoceptor density was increased in the renal cortex of SHB and SBN rats. In contrast, cerebral alpha 2-adrenoceptor densities were markedly decreased in SBN but unchanged in SBH rats. Blood pressure increased only after five weeks of high sodium diet, in SBH and to a lesser extent in SBN rats. The change in alpha 2-adrenoceptor densities thus preceded the blood pressure elevation. The dietary sodium-induced increase in renal alpha 2-adrenoceptor densities which precedes the blood pressure elevation does not appear to be a genetic marker of hypertension. Conversely, the marked decrease of cerebral alpha 2-adrenoceptors in SBN rats may represent an adaptative change in sympathetic activity responsible for the resistance to the development of salt-induced hypertension.
脑和肾的α2-肾上腺素能受体分别参与交感神经活动的控制和钠重吸收的调节，且在体外受钠离子的调节。本研究的目的是探究高钠饮食（8%）与正常钠饮食（0.2%）对Sabra高血压大鼠（SBH）和正常血压大鼠（SBN）脑和肾α-肾上腺素能受体的影响。在高钠饮食两周或五周后，SHB和SBN大鼠肾皮质中的α2-肾上腺素能受体密度增加。相比之下，SBN大鼠脑内α2-肾上腺素能受体密度显著降低，而SBH大鼠脑内α2-肾上腺素能受体密度无变化。仅在高钠饮食五周后，SBH大鼠血压升高，SBN大鼠血压升高程度较小。因此，α2-肾上腺素能受体密度的变化先于血压升高。饮食钠诱导的肾α2-肾上腺素能受体密度增加先于血压升高，这似乎不是高血压的遗传标记。相反，SBN大鼠脑内α2-肾上腺素能受体显著减少可能代表交感神经活动的适应性变化，这导致了对盐诱导高血压发展的抵抗。
