Shi S J, Preuss H G, Abernethy D R, Li X, Jarrell S T, Andrawis N S
Department of Medicine, Georgetown University Medical Center, Washington, D.C. 20007, USA.
J Hypertens. 1997 Aug;15(8):857-62. doi: 10.1097/00004872-199715080-00009.
To determine the changes in serum angiotensin II (Ang II) and endothelin-1 levels induced by vanadium treatment of sugar-fed rats in order to investigate the relationship between changes in blood pressure and Ang II and endothelin-1 levels.
Male spontaneously hypertensive rats (SHR) were fed starch (control), sucrose, and sucrose plus vanadium compounds at various concentrations. The systolic blood pressure of the rats was estimated by tail-cuff plethysmography. Serum Ang II and endothelin-1 levels were measured by radioimmunoassay.
There were increases in systolic blood pressure (by 8%) and in serum Ang II (by 20%) in sucrose-fed SHR compared with control. In sucrose plus vanadium-fed SHR, the lowering of the systolic blood pressure (by 11-16% of the sucrose-fed value) was accompanied by a significant decrease in Ang II levels (by 25-60% of the sucrose-fed value) and an increase in endothelin-1 level (by 61-76% of the sucrose-fed value).
That Ang II levels are elevated in sucrose-induced hypertension and decreased after vanadium therapy suggests that the renin-angiotensin system plays a role in the induction of hypertension in this model. On the other hand, the elevation of endothelin-1 levels associated with a decreased systolic blood pressure might be secondary to vanadium stimulation of endothelial cells. The data suggest that endothelin-1 is not involved in sugar-induced elevations of the blood pressure.
测定钒处理食糖大鼠后血清血管紧张素II（Ang II）和内皮素-1水平的变化，以研究血压变化与Ang II和内皮素-1水平之间的关系。
将雄性自发性高血压大鼠（SHR）分别喂食淀粉（对照组）、蔗糖以及添加不同浓度钒化合物的蔗糖。采用尾套体积描记法估计大鼠的收缩压。通过放射免疫分析法测定血清Ang II和内皮素-1水平。
与对照组相比，喂食蔗糖的SHR收缩压升高（8%），血清Ang II升高（20%）。在喂食蔗糖加钒的SHR中，收缩压降低（降低幅度为喂食蔗糖组数值的11%-16%），同时Ang II水平显著降低（降低幅度为喂食蔗糖组数值的25%-60%），内皮素-1水平升高（升高幅度为喂食蔗糖组数值的61%-76%）。
蔗糖诱导的高血压中Ang II水平升高，钒治疗后降低，这表明肾素-血管紧张素系统在该模型高血压的诱导中起作用。另一方面，内皮素-1水平升高伴随收缩压降低可能是钒刺激内皮细胞的继发结果。数据表明内皮素-1不参与食糖诱导的血压升高。
