Effect of the Essential Trace Element, Zinc, on Blood Pressure and Circulation.

为了探讨必需微量元素锌对血压和血液循环的影响，我们观察了锌缺乏症大鼠的血压和肾脏血流动力学。首先，我们发现原本健康的缺锌大鼠血压没有明显变化，但肾血管阻力明显增加，肾血压下降。然后，我们研究了机理。为了探讨一氧化氮（NO）是否参与了这一机制，我们观察了NO合成酶（NOS）抑制剂L-NAME和NO供体硝普钠（SNP）对锌缺乏对肾脏血流动力学的影响。L-NAME （iv）对缺锌大鼠的影响与对照组相似，提示NOS在其机制中作用不大。另一方面，过量NO同时注射大量SNP可显著降低对照组与缺锌大鼠肾脏血流动力学的差异。这一事实表明，一氧化氮的缺乏增加了锌缺乏症的肾血管阻力。综上所述，锌缺乏增加肾血管阻力的机制主要是No而非NOS。此外，我们观察到锌缺乏大鼠肾脏中Cu/Zn超氧化物歧化酶的活性明显低于对照组。提示超氧化物（O^<2->）的局部活化在该机制中起一定作用。此外，血管紧张素-1转换酶抑制剂依那普利对锌缺乏对肾脏血流动力学的影响无显著影响，提示肾素-血管紧张素系统在该机制中的作用不大。

To investigate the effects of the essential trace element, zinc, on blood pressure and circulation, we observed blood pressure and renal hemodynamics on rats induced zinc deficiency. First, we found that no significant changes in blood pressure but significant increments in renal vascular resistance and decrements in renal blood pressure in zinc-deficient rats that were originally healthy. Then, we studied the mechanism. To investigate whether nitric oxide (NO) is responsible for the mechanism, we observed the influences of the NO synthase (NOS) inhibitor, L-NAME, and the NO donor, sodium nitroprusside (SNP), on the effects of zinc deficiency on renal hemodynamics. Administration of L-NAME (iv) had similar effects on zinc-deficient rats to on controls, suggesting that NOS plays little roles on the mechanism. On the other hand, administration of excessive NO with injection of much SNP significantly reduces the differences of renal hemodynamics between controls and zinc-deficient rats. The fact implies that the shortage of NO increases renal vascular resistance in zinc deficiency. Taken together, it was suggested that No but not NOS was responsible for the mechanism by which zinc deficiency increases renal vascular resistance. Furthermore, we observed that the activities of Cu/Zn superoxide dismutase was significantly lower in kidneys of zinc-deficient rats compared to controls. It suggested that local activation of superoxide (O^<2->) plays some role in the mechanism. Additionally, the angiotensin-1 converting enzyme inhibitor, enalapril, had no significant influences on the effect of zinc deficiency on renal hemodynamics, suggesting that the responsibilities of renin-angiotensin system for the mechanism was little.