| Budget Amount *help |
¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2000: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1999: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Research Abstract |
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.
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