Nitric oxide production decreases after salt loading but is not related to blood pressure changes or nitric oxide-mediated vascular responses
Nitric oxide production decreases after salt loading but is not related to blood pressure changes or nitric oxide-mediated vascular responses
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DOI：
10.1097/00004872-200301000-00025
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发表时间：
2003-01-01
影响因子：
4.9
通讯作者：
Stein, CM
中科院分区：
文献类型：
--
作者：
Dishy, V;Sofowora, GG;Stein, CM
背景 一氧化氮的产生是一种稳态机制，可以在盐负荷期间调节血压。动物模型和人类中的盐敏感性高血压的特征是盐负荷后血压升高和一氧化氮生成减少。目前尚不清楚这种一氧化氮生成受损是否是高血压的结果，还是导致血压对盐产生反应的机制。 方法和结果 25 名血压正常的受试者在接受高盐饮食（400 mmol/天）或低盐饮食（10 mmol/天）、低硝酸盐饮食 6 天后，测量了盐负荷对血压、一氧化氮介导的血管舒张和一氧化氮生成的影响。高盐饮食期间平均动脉压升高[4 12 名受试者中 +/- 1 mmHg（平均 SEM）]，13 名受试者中保持不变或下降（-4 +/- 1 mmHg）。血浆亚硝酸盐和硝酸盐（衡量一氧化氮生成量的指标）从低盐饮食期间的 39 +/- 3.3 mumol/l 显着下降至高盐饮食期间的 22.4 +/- 2.4 mumol/l (P = 0.0001)。然而，从低盐饮食到高盐饮食的平均动脉压变化与血浆亚硝酸盐和硝酸盐的变化无关（r = 0.14，P = 0.51）。前臂血流量因精神压力（一氧化氮介导的反应）而显着增加（P < 0.0001），但不受钠摄入量的影响（低盐期间每 100 毫升 7.8 +/- 0.9 至 11.2 +/- 1.4 毫升/分钟，高盐期间每 100 毫升 8.5 +/- 1.2 至 10.4 +/- 1.3 毫升/分钟 P = 0.3).结论盐负荷导致盐敏感和耐盐正常血压受试者一氧化氮生成减少，这与血压变化无关，并且不影响一氧化氮介导的血管对精神应激的反应。与耐盐动物模型相比，健康受试者的盐负荷不会增加一氧化氮的产生。因此，血压对盐负荷的增加可能是通过一氧化氮以外的机制发生的，或者盐敏感个体对盐敏感和耐盐受试者在盐负荷后发生的一氧化氮生成减少更敏感。 (C) 2003 年利平科特·威廉姆斯·威尔金斯。
Background Nitric oxide production is a homeostatic mechanism that may regulate blood pressure during salt loading. Salt-sensitive hypertension in animal models and in humans is characterized by increased blood pressure and decreased nitric oxide production after salt loading. It is not known if this impaired nitric oxide production is the result of hypertension or is a mechanism contributing to the blood pressure response to salt.Methods and results The effects of salt loading on blood pressure, nitric oxide-mediated vasodilation and nitric oxide production were measured in 25 normotensive subjects after 6 days on either a high (400 mmol/day) or low (10 mmol/day) sodium, low nitrate diet Mean arterial pressure increased during the high-salt diet [4 +/- 1 mmHg (mean SEM)] in 12 subjects and remained unchanged or decreased (-4 +/- 1 mmHg) in 13 subjects. Plasma nitrite and nitrate, a measure of nitric oxide production, decreased significantly from 39 +/- 3.3 mumol/l during the low-salt diet to 22.4 +/- 2.4 mumol/l during the high-salt diet (P = 0.0001). However, changes in mean arterial pressure from low- to high-salt diet did not correlate with changes in plasma nitrite and nitrate (r= 0.14, P = 0.51). Forearm blood flow increased significantly (P < 0.0001) in response to mental stress, a nitric oxide-mediated response, but was not affected by sodium intake (from 7.8 +/- 0.9 to 11.2 +/- 1.4 ml/min per 100 ml during low salt versus 8.5 +/- 1.2 to 10.4 +/- 1.3 ml/min per 100 ml during high salt P = 0.3).Conclusions Salt loading results in a decrease in nitric oxide production in both salt-sensitive and salt-resistant normotensive subjects, which is independent of changes in blood pressure and does not affect the nitric oxide-mediated vascular response to mental stress. In contrast to salt-resistant animal models, salt loading in healthy subjects does not increase nitric oxide production. Therefore, the increased blood pressure response to salt loading may occur through mechanisms other than nitric oxide, or salt-sensitive individuals are more sensitive to the reduced nitric oxide production that occurs after salt loading in both salt-sensitive and salt-resistant subjects. (C) 2003 Lippincott Williams Wilkins.