Campese V M, Tawadrous M, Bigazzi R, Bianchi S, Mann A S, Oparil S, Raij L
University of Southern California, Los Angeles, USA.
Hypertension. 1996 Sep;28(3):335-40. doi: 10.1161/01.hyp.28.3.335.
In response to a high salt intake, salt-sensitive hypertensive individuals retain more sodium and manifest a rise in blood pressure greater than that in salt-resistant individuals. In this study, we tested whether salt sensitivity might be related at least in part to reduced secretion of atrial natriuretic peptide (ANP) or to abnormal nitric oxide production. We measured plasma ANP and NO2+NO3 in 7 normotensive individuals and 13 salt-sensitive and 14 salt-resistant blacks with essential hypertension under conditions of low (10 mEq/d) and high (250 mEq/d) salt intake. To evaluate possible racial differences in ANP secretion, we also measured plasma ANP in 6 salt-sensitive and 8 salt-resistant hypertensive whites during low and high salt intakes. Under low salt conditions, plasma ANP levels were not different in normotensive control subjects and salt-sensitive and salt-resistant hypertensive blacks. During high salt intake, plasma ANP levels did not change in control subjects and salt-resistant patients but decreased in salt-sensitive patients. ANP levels after high salt diet were lower (P < .01) in salt-sensitive than salt-resistant blacks. In hypertensive whites, high salt intake caused no significant change in plasma ANP. Under low salt conditions, plasma NO2+NO3 levels were higher (P < .05) in salt-sensitive (189 +/- 7.9 mumol/L) and salt-resistant (195 +/- 13.5 mumol/L) black patients than in control subjects (108 +/- 9.7 mumol/L). During high salt intake, plasma NO2+NO3 decreased significantly (P < .01) in both salt-sensitive (150 +/- 7.0 mumol/L) and salt-resistant (142 +/- 9.0 mumol/L) patients. These studies show that under conditions of high salt intake, salt-sensitive hypertensive blacks manifest a paradoxical decrease in ANP secretion. This abnormality may play a role in the reduced ability of these individuals to excrete a sodium load and in the sodium-induced rise in blood pressure. This study does not support the hypothesis that salt sensitivity depends on a deficit of nitric oxide production, but it suggests that high salt intake may alter the endothelium-dependent adaptation of peripheral resistance vessels.
对于高盐摄入，盐敏感型高血压个体潴留更多的钠，且血压升高幅度大于盐抵抗型个体。在本研究中，我们测试了盐敏感性是否至少部分与心房利钠肽（ANP）分泌减少或一氧化氮生成异常有关。我们测量了7名血压正常个体以及13名盐敏感型和14名盐抵抗型原发性高血压黑人在低盐（10 mEq/d）和高盐（250 mEq/d）摄入情况下的血浆ANP和NO2+NO3水平。为了评估ANP分泌可能存在的种族差异，我们还测量了6名盐敏感型和8名盐抵抗型高血压白人在低盐和高盐摄入期间的血浆ANP水平。在低盐条件下，血压正常的对照受试者以及盐敏感型和盐抵抗型高血压黑人的血浆ANP水平没有差异。在高盐摄入期间，对照受试者和盐抵抗型患者的血浆ANP水平没有变化，但盐敏感型患者的血浆ANP水平下降。高盐饮食后，盐敏感型黑人的ANP水平低于盐抵抗型黑人（P <.01）。在高血压白人中，高盐摄入导致血浆ANP没有显著变化。在低盐条件下，盐敏感型（189±7.9 μmol/L）和盐抵抗型（195±13.5 μmol/L）黑人患者的血浆NO2+NO3水平高于对照受试者（108±9.7 μmol/L）（P <.05）。在高盐摄入期间，盐敏感型（150±7.0 μmol/L）和盐抵抗型（142±9.0 μmol/L）患者的血浆NO2+NO3均显著下降（P <.01）。这些研究表明，在高盐摄入情况下，盐敏感型高血压黑人表现出ANP分泌的反常减少。这种异常可能在这些个体排泄钠负荷能力降低以及钠诱导的血压升高中起作用。本研究不支持盐敏感性取决于一氧化氮生成不足的假说，但表明高盐摄入可能改变外周阻力血管的内皮依赖性适应性。
