Dustan H P
J Cardiovasc Pharmacol. 1985;7 Suppl 8:S56-63.
To test the hypothesis that salt-sensitive hypertension reflects an abnormal response of the sympathetic nervous system (SNS) to salt, arterial pressure and plasma norepinephrine (NE) concentration were measured in 23 black hypertensive patients and 28 black normotensive control subjects during 4 days of salt depletion and 3 days of salt loading. When the sequence was salt depletion followed by salt loading, plasma NE rose with salt depletion and was suppressed by salt loading. In normotensive subjects, plasma NE with salt loading returned to control values, but in hypertensive patients it remained elevated suggesting SNS stimulation by the salt load. Plasma NE responses of hypertensive patients did not distinguish between those who became normotensive with salt depletion from those who did not. The sequence was reversed with salt loading preceding salt depletion, to investigate further these abnormal plasma NE responses to salt loading. With this sequence, plasma NE was only slightly and insignificantly reduced by salt loading and responses of hypertensive patients were similar to those of normotensive subjects. In contrast, plasma NE rose with salt depletion as before. With both protocols plasma NE correlated inversely with urinary sodium excretion as previously described. These results in black hypertensive patients are not consonant with those obtained in other studies of primarily white hypertensive patients, suggesting that salt-sensitive hypertension may have a different mechanism in blacks than in whites.
为了验证盐敏感性高血压反映交感神经系统(SNS)对盐的异常反应这一假说,在23名黑人高血压患者和28名黑人血压正常的对照受试者进行4天限盐和3天高盐饮食期间,测量了动脉血压和血浆去甲肾上腺素(NE)浓度。当顺序为限盐后高盐饮食时,血浆NE随着限盐而升高,并在高盐饮食时受到抑制。在血压正常的受试者中,高盐饮食时血浆NE恢复到对照值,但在高血压患者中仍保持升高,提示盐负荷刺激了SNS。高血压患者的血浆NE反应无法区分限盐后血压恢复正常的患者和未恢复正常的患者。将顺序颠倒,先进行高盐饮食再限盐,以进一步研究这些对高盐饮食异常的血浆NE反应。采用此顺序时,高盐饮食仅使血浆NE略有降低且无统计学意义,高血压患者的反应与血压正常的受试者相似。相比之下,血浆NE如之前一样随着限盐而升高。两种方案下,血浆NE均与尿钠排泄呈负相关,如先前所述。黑人高血压患者的这些结果与其他主要针对白人高血压患者的研究结果不一致,表明盐敏感性高血压在黑人中的机制可能与白人不同。