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钠盐对盐敏感男性升压反应性的影响。

Effects of sodium salts on pressor reactivity in salt-sensitive men.

作者信息

Sharma A M, Schattenfroh S, Thiede H M, Oelkers W, Distler A

机构信息

Department of Internal Medicine, Universitätsklinikum Steglitz, Free University of Berlin, FRG.

出版信息

Hypertension. 1992 Jun;19(6 Pt 1):541-8. doi: 10.1161/01.hyp.19.6.541.

DOI:10.1161/01.hyp.19.6.541
PMID:1592448
Abstract

Blood pressure in patients with essential hypertension is raised by sodium chloride but not by nonchloride sodium salts. Although a high sodium chloride diet is known to augment the pressor response to norepinephrine and angiotensin II, the effect of nonchloride sodium salts on pressor responsiveness has not been studied so far. To examine whether sodium chloride and nonchloride sodium salts evoke different pressor responses to these agonists, we performed graded norepinephrine and angiotensin II infusions in salt-sensitive (n = 7) and salt-resistant (n = 8) normotensive subjects. The subjects were given a low salt diet (20 mmol/day) for 3 weeks, to which a supplement of 200 mmol sodium per day, provided as either sodium chloride or sodium citrate, or a placebo was added for 1 week each. We found that, although sodium chloride raised mean arterial blood pressure in the salt-sensitive subjects (p less than 0.005), sodium citrate did not. However, under both sodium salts pressor response to norepinephrine and angiotensin II was significantly greater than under placebo (p less than 0.02). Furthermore, with both sodium salts, pressor response in the salt-sensitive subjects was greater than in the salt-resistant subjects (p less than 0.01). This study thus demonstrates that, although blood pressure in salt-sensitive individuals is raised by sodium chloride only, both sodium chloride and sodium citrate evoke similar increases in pressor response to norepinephrine and angiotensin II. Since pressor response increased with both sodium salts but resting blood pressure increased only with sodium chloride, enhanced pressor responsiveness alone cannot account for the sodium chloride-induced rise in resting blood pressure.

摘要

原发性高血压患者的血压会因氯化钠升高,但不会因非氯化物钠盐升高。尽管已知高氯化钠饮食会增强对去甲肾上腺素和血管紧张素II的升压反应,但到目前为止尚未研究非氯化物钠盐对升压反应性的影响。为了研究氯化钠和非氯化物钠盐对这些激动剂是否引发不同的升压反应,我们对盐敏感(n = 7)和盐抵抗(n = 8)的血压正常受试者进行了去甲肾上腺素和血管紧张素II的分级输注。受试者接受低盐饮食(20 mmol/天)3周,然后每天补充200 mmol钠,分别以氯化钠或柠檬酸钠的形式提供,或添加安慰剂,每种持续1周。我们发现,尽管氯化钠使盐敏感受试者的平均动脉血压升高(p < 0.005),但柠檬酸钠没有。然而,在两种钠盐情况下,对去甲肾上腺素和血管紧张素II的升压反应均显著大于安慰剂组(p < 0.02)。此外,在两种钠盐情况下,盐敏感受试者的升压反应均大于盐抵抗受试者(p < 0.01)。因此,本研究表明,尽管盐敏感个体的血压仅因氯化钠升高,但氯化钠和柠檬酸钠对去甲肾上腺素和血管紧张素II的升压反应均引发类似的增加。由于两种钠盐都使升压反应增加,但静息血压仅在氯化钠作用下升高,因此仅升压反应性增强不能解释氯化钠引起的静息血压升高。

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