新浪登录
腾讯登录Circulation：食盐过多损伤血管？
| 导读 | 最新发表在<em>Circulation</em>杂志上的一项研究证实：食盐摄入过多会损害血管，亦会升高血压。
<p align="center"><img src="http://www.bioon.com/biology/UploadFiles/201206/2012061909460649.jpg" alt=... |
最新发表在<em>Circulation</em>杂志上的一项研究证实：食盐摄入过多会损害血管，亦会升高血压。
<p align="center"><img src="http://www.bioon.com/biology/UploadFiles/201206/2012061909460649.jpg" alt="" width="512" height="384" border="0" /></p>
<!--more-->
在文章背景资料中，作者解释说：血压正常的人，高盐饮食几乎对血压没有急性危害。但是，这并不完全理解为什么高钠（盐）的长期摄入可导致高血压的原因。研究推测慢性高盐摄入量的人血清尿酸和尿白蛋白排泄量更高，他们还推测这些生物标志物高水平预示血管内皮功能障碍，将会导致高血压。
John P. Forman和团队检测了5556名荷兰成年男性和女性的钠（盐）摄入量。
他们发现高含量、长期钠摄入量的人往往尿酸和白蛋白水平更高，这两种标志物为血管损伤标志。
他们的研究证实尿酸水平以及白蛋白与高血压风险之间密切相关。
<div id="ztload">
<div>
<div>
<img src="http://www.bioon.com/biology/UploadFiles/201206/2012061909452594.gif" alt="" width="115" height="150" border="0" />
<a title="" href="http://dx.doi.org/10.1161/CIRCULATIONAHA.112.096115" target="_blank">doi:10.1161/CIRCULATIONAHA.112.096115</a>
PMC:
PMID:
</div>
<div>
<br/><strong>Association between Sodium Intake and Change in Uric Acid, Urine Albumin Excretion, and the Risk of Developing Hypertension</strong><br/>
John P. Forman*;Lieneke Scheven;Paul E. de Jong;Stephan J.L. Bakker;Gary C. Curhan1;Ron T. Gansevoort
<p id="p-1"><br/><strong><em>Background</em></strong><br/>
—In non-hypertensive individuals, a high sodium diet has little acute effect on blood pressure but, for unclear reasons, is associated with hypertension if consumed chronically. We hypothesized that a chronically high sodium intake would be associated with increases in biomarkers of endothelial dysfunction, specifically serum uric acid (SUA) and urine albumin excretion (UAE), and that high sodium intake would be associated with incident hypertension among those with higher SUA and UAE.</p>
<p id="p-2"><br/><strong><em>Methods and Results</em></strong><br/>
—We prospectively analyzed the associations between sodium intake and the change in SUA (N=4062) and UAE (N=4146) among participants of the PREVEND study who were not taking antihypertensive medications. We also examined the association of sodium intake with the incidence of hypertension (N=5556) among non-hypertensive participants. After adjusting for confounders, each 1 gram higher sodium intake was associated with a 1.2μmol/L increase in SUA ( p=0.01) and a 4.6mg/d increase in UAE (p<0.001). The relation between sodium intake and incident hypertension varied according to SUA and UAE. For each 1 gram higher sodium intake, the adjusted hazard ratio for developing hypertension was 0.98 (0.89-1.08) among those in the lowest tertile of SUA, and 1.09 (1.02-1.16) among those in the highest. Corresponding hazard ratios were 0.99 (0.93-1.06) among participants whose UAE was <10mg/d, and 1.18 (1.07-1.29) among those whose UAE was >15mg/d.</p>
<p id="p-3"><br/><strong><em>Conclusions</em></strong><br/>
—Over time, higher sodium intake is associated with increases in SUA and UAE. Among individuals with higher SUA and urine UAE, a higher sodium intake is an independent risk factor for developing hypertension.</p>
<br/>来源：生物谷
</div>
</div>
</div>
<p align="center"><img src="http://www.bioon.com/biology/UploadFiles/201206/2012061909460649.jpg" alt="" width="512" height="384" border="0" /></p>
<!--more-->
在文章背景资料中，作者解释说：血压正常的人，高盐饮食几乎对血压没有急性危害。但是，这并不完全理解为什么高钠（盐）的长期摄入可导致高血压的原因。研究推测慢性高盐摄入量的人血清尿酸和尿白蛋白排泄量更高，他们还推测这些生物标志物高水平预示血管内皮功能障碍，将会导致高血压。
John P. Forman和团队检测了5556名荷兰成年男性和女性的钠（盐）摄入量。
他们发现高含量、长期钠摄入量的人往往尿酸和白蛋白水平更高，这两种标志物为血管损伤标志。
他们的研究证实尿酸水平以及白蛋白与高血压风险之间密切相关。
<div id="ztload">
<div>
<div>
<img src="http://www.bioon.com/biology/UploadFiles/201206/2012061909452594.gif" alt="" width="115" height="150" border="0" />
<a title="" href="http://dx.doi.org/10.1161/CIRCULATIONAHA.112.096115" target="_blank">doi:10.1161/CIRCULATIONAHA.112.096115</a>
PMC:
PMID:
</div>
<div>
<br/><strong>Association between Sodium Intake and Change in Uric Acid, Urine Albumin Excretion, and the Risk of Developing Hypertension</strong><br/>
John P. Forman*;Lieneke Scheven;Paul E. de Jong;Stephan J.L. Bakker;Gary C. Curhan1;Ron T. Gansevoort
<p id="p-1"><br/><strong><em>Background</em></strong><br/>
—In non-hypertensive individuals, a high sodium diet has little acute effect on blood pressure but, for unclear reasons, is associated with hypertension if consumed chronically. We hypothesized that a chronically high sodium intake would be associated with increases in biomarkers of endothelial dysfunction, specifically serum uric acid (SUA) and urine albumin excretion (UAE), and that high sodium intake would be associated with incident hypertension among those with higher SUA and UAE.</p>
<p id="p-2"><br/><strong><em>Methods and Results</em></strong><br/>
—We prospectively analyzed the associations between sodium intake and the change in SUA (N=4062) and UAE (N=4146) among participants of the PREVEND study who were not taking antihypertensive medications. We also examined the association of sodium intake with the incidence of hypertension (N=5556) among non-hypertensive participants. After adjusting for confounders, each 1 gram higher sodium intake was associated with a 1.2μmol/L increase in SUA ( p=0.01) and a 4.6mg/d increase in UAE (p<0.001). The relation between sodium intake and incident hypertension varied according to SUA and UAE. For each 1 gram higher sodium intake, the adjusted hazard ratio for developing hypertension was 0.98 (0.89-1.08) among those in the lowest tertile of SUA, and 1.09 (1.02-1.16) among those in the highest. Corresponding hazard ratios were 0.99 (0.93-1.06) among participants whose UAE was <10mg/d, and 1.18 (1.07-1.29) among those whose UAE was >15mg/d.</p>
<p id="p-3"><br/><strong><em>Conclusions</em></strong><br/>
—Over time, higher sodium intake is associated with increases in SUA and UAE. Among individuals with higher SUA and urine UAE, a higher sodium intake is an independent risk factor for developing hypertension.</p>
<br/>来源：生物谷
</div>
</div>
</div>
还没有人评论，赶快抢个沙发