Yamazaki H, Yoshimura M, Kambara S, Lee L C, Fukuyama M, Sasaki S, Takahashi H, Takeda K, Ijichi H
Jpn Circ J. 1986 May;50(5):442-8. doi: 10.1253/jcj.50.442.
To analyze the conflicting data on the relationship between sodium intake and sympathetic activity, the effects of a chronically excessive intake of sodium on renal sympathetic activity and blood pressure were investigated in normotensive rats. Renal sympathetic activity was estimated by urinary excretion of free norepinephrine (NE) and the turnover of NE in the kidneys. Blood pressure increased in rats receiving a high sodium diet when compared with that of the basal sodium diet. Urinary-free NE, epinephrine (E) and dopamine (DA) excretions in rats receiving a high sodium diet were enhanced significantly from those in the basal sodium diet. The turnover of NE in the kidneys was more enhanced in the high sodium group than in the basal sodium group. By blocking the sympathetic tone with ganglionic blockade, hexamethonium, enhanced excretion of urinary NE and elevation of blood pressure in response to salt loading were blocked to the levels of the basal sodium diet. These results suggest that a chronically excessive intake of sodium enhances the renal sympathetic and adreno-medullary activities, leading to a rise in blood pressure in normotensive rats.
为分析关于钠摄入与交感神经活动之间关系的相互矛盾的数据,我们在正常血压大鼠中研究了长期过量摄入钠对肾交感神经活动和血压的影响。通过尿中游离去甲肾上腺素(NE)的排泄及肾内NE的周转率来评估肾交感神经活动。与基础钠饮食组相比,接受高钠饮食的大鼠血压升高。接受高钠饮食的大鼠尿中游离NE、肾上腺素(E)和多巴胺(DA)的排泄量较基础钠饮食组显著增加。高钠组肾内NE的周转率比基础钠组增强更明显。通过用神经节阻滞剂六甲铵阻断交感神经张力,盐负荷引起的尿NE排泄增加和血压升高被阻断至基础钠饮食组的水平。这些结果表明,长期过量摄入钠会增强肾交感神经和肾上腺髓质活动,导致正常血压大鼠血压升高。