Free radical scavenging reverses fructose-induced salt-sensitive hypertension.
Free radical scavenging reverses fructose-induced salt-sensitive hypertension.
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DOI：
10.2147/ibpc.s147674
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发表时间：
2018
影响因子：
2.2
通讯作者：
Beierwaltes WH
中科院分区：
文献类型：
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作者：
Zenner ZP;Gordish KL;Beierwaltes WH
我们以前曾报道，适量补充20%的果糖而不是葡萄糖会导致盐敏感型高血压，这与近端钠氢交换活性增加和肾脏钠滞留增加有关。我们还发现，虽然高盐增加了肾脏一氧化氮的形成，但在摄入果糖的情况下，这一过程会受到抑制。我们推测，导致果糖诱导的盐敏性高血压的至少部分途径可能是由于果糖诱导的活性氧物种的形成和肾素分泌的不适当刺激，所有这些都会导致血压升高。我们发现，摄入20%的果糖和高盐饮食都会刺激8-异前列腺素的排泄。模拟超氧化物歧化酶(SOD)的Tempoll显著减少了这种升高的排泄。接下来，我们将大鼠置于高盐饮食(4%)和正常饮食或20%果糖的基础上持续1周，无论是否长期服用坦普尔。果糖加高盐饮食导致血压迅速升高(15毫米汞柱)，并逆转了高盐对血浆肾素活性的抑制。坦普尔可逆转升压反应，恢复肾素的高盐抑制。我们得出结论，果糖诱导的盐敏性高血压是由与盐滞留相关的肾脏活性氧形成增加和肾素-血管紧张素系统增强所驱动的。
We have previously reported that a moderate dietary supplementation of 20% fructose but not glucose leads to a salt-sensitive hypertension related to increased proximal sodium–hydrogen exchanger activity and increased renal sodium retention. We also found that while high salt increased renal nitric oxide formation, this was retarded in the presence of fructose intake. We hypothesized that at least part of the pathway leading to fructose-induced salt-sensitive hypertension could be due to fructose-induced formation of reactive oxygen species and inappropriate stimulation of renin secretion, all of which would contribute to an increase in blood pressure. We found that both 20% fructose intake and a high-salt diet stimulated 8-isoprostane excretion. The superoxide dismutase (SOD) mimetic tempol significantly reduced this elevated excretion. Next, we placed rats on a high-salt diet (4%) for 1 week in combination with normal rat chow or 20% fructose with or without chronic tempol administration. A fructose plus high-salt diet induced a rapid increase (15 mmHg) in systolic blood pressure and reversed high salt suppression of plasma renin activity. Tempol treatment reversed the pressor response and restored high salt suppression of renin. We conclude that fructose-induced salt-sensitive hypertension is driven by increased renal reactive oxygen species formation associated with salt retention and an enhanced renin–angiotensin system.