Hemodynamics and Salt-and-Water Balance Link Sodium Storage and Vascular Dysfunction in Salt-Sensitive Subjects.
Hemodynamics and Salt-and-Water Balance Link Sodium Storage and Vascular Dysfunction in Salt-Sensitive Subjects.
复制标题
DOI：
10.1161/hypertensionaha.116.07289
复制
发表时间：
2016-07
期刊：
影响因子：
--
通讯作者：
Elijovich F
中科院分区：
文献类型：
--
作者：
Laffer CL;Scott RC 3rd;Titze JM;Luft FC;Elijovich F
我们研究了8名盐敏感（SS）和13名盐抵抗（SR）血压正常志愿者的24小时血流动力学变化。盐负荷后，SS组平均动脉压（MAP）升高，（96.5±2.8）比SR（84.2±2.7 mmHg），p<0.01，由于SS的总外周阻力（TPR）较高（1791±148）比SR（1549±66 dyn.cm−5.sec−1），p=0.05，而心输出量（CO）组间无差异（SS 4.5±0.3 vs SR 4.4±0.2 l/min，ns）。在盐耗尽后，两组的CO同样减少。SR组TPR增加24±6%（p<0.001），而MAP无变化。相反，在SS中TPR没有变化（1± 6%，ns）。因此，他们的MAP降低，消除了组间的MAP差异。在方案的两个阶段，SS的E/e'比高于SR。在这21例受试者和32例高血压患者中，盐负荷或耗竭期间SR和SS的Na+平衡相似。然而，SR在盐保留期间没有增加体重（-158 ±250 g），而SS增加了体重（819±204），与等渗性水保留相当。在盐消耗期间，SR失去了等渗Na+排泄的预期重量，而SS失去了更大的重量，未能完全纠正前一天的液体潴留。我们的结论是SS是无法调节TPR响应盐耗竭，反映他们无法血管舒张响应盐负荷。我们认为，SS和SR之间的水平衡的差异表明盐和水的存储在间质室，可能与SS的血管功能障碍的差异。
We investigated 24-hour hemodynamic changes produced by salt loading and depletion in eight salt-sensitive (SS) and 13 salt-resistant (SR) normotensive volunteers. After salt loading, mean arterial pressure (MAP) was higher in SS (96.5±2.8) than SR (84.2±2.7 mmHg), p<0.01, owing to higher total peripheral resistance (TPR) in SS (1791±148) than SR (1549±66 dyn.cm−5.sec−1), p=0.05, whereas cardiac output (CO) was not different between groups (SS 4.5±0.3 vs SR 4.4±0.2 l/min, ns). Following salt depletion, CO was equally reduced in both groups. TPR increased 24±6% (p<0.001) in SR, whose MAP remained unchanged. In contrast, TPR did not change in SS (1±6%, ns). Thus, their MAP was reduced, abolishing the MAP difference between groups. SS had higher E/e’ ratios than SR in both phases of the protocol. In these 21 subjects and in 32 hypertensive patients, Na+ balance was similar in SR and SS during salt loading or depletion. However, SR did not gain weight during salt retention (−158±250 g), whereas SS did (819±204), commensurate to isoosmolar water retention. During salt depletion, SR lost the expected amount of weight for isoosmolar Na+ excretion, whereas SS lost a greater amount that failed to fully correct the fluid retention from the previous day. We conclude that SS are unable to modulate TPR in response to salt depletion, mirroring their inability to vasodilate in response to salt loading. We suggest that differences in water balance between SS and SR indicate differences in salt-and-water storage in the interstitial compartment that may relate to vascular dysfunction in SS.