Omvik P, Gerdts E, Myking O, Lund-Johansen P
Department of Cardiology, Haukeland Hospital, Bergen, Norway.
Blood Press. 1999;8(4):233-41. doi: 10.1080/080370599439625.
Salt may be involved in the pathogenesis of essential hypertension but no agreement has been reached on how salt might exert its blood pressure control. One reason for the conflicting results could be differences in response to changes in salt intake--i.e. between salt-sensitive and salt-resistant subjects. Hypertension reflects a hemodynamic disturbance: mainly an increase in total peripheral resistance. In order to determine whether central hemodynamics is different in salt-sensitive and salt-resistant essential hypertension, a study was carried out on 37 patients aged 31-63 years with mean casual blood pressure 165/104 mmHg. Based on an increase in ambulatory 24-h mean blood pressure of > or = 10% after one week of dietary salt loading (260 mmol NaCl/24 h) following a one-week salt depletion period (60 mmol NaCl/24 h), 7 patients (19%) were classified as salt sensitive and 30 patients (81%) as salt resistant. Before the salt-sensitivity test, while patients were on their habitual salt intake (160 mmol NaCl/24 h), central hemodynamics (intra-arterial pressure, cardiac output by dye dilution, heart rate by electrocardiogram, and total peripheral resistance) was examined at rest and during bicycle exercise. None of the central hemodynamic variables were different between the two groups, despite a marked difference in blood pressure response to one week of salt loading between the salt-sensitive and the salt-resistant groups (27/9 mmHg vs -2/1 mmHg). Furthermore, no statistically significant differences were observed in neurohumoral variables or echocardiographic indices of left ventricular dimensions between the two groups. Owing to the invasive hemodynamic procedure, central hemodynamics was not restudied during high- or low salt intake. It is concluded that there is no difference in central hemodynamics in salt-sensitive and salt-resistant hypertensive patients when they are on their habitual salt diet.
盐可能参与原发性高血压的发病机制，但关于盐如何发挥其血压调控作用尚未达成共识。结果相互矛盾的一个原因可能是对盐摄入量变化的反应存在差异，即盐敏感者和盐抵抗者之间的差异。高血压反映了一种血液动力学紊乱：主要是总外周阻力增加。为了确定盐敏感型和盐抵抗型原发性高血压患者的中枢血液动力学是否不同，对37例年龄在31 - 63岁之间、平均偶测血压为165/104 mmHg的患者进行了一项研究。在经过一周的低盐饮食期（60 mmol氯化钠/24小时）后，进行一周的高盐饮食（260 mmol氯化钠/24小时），根据动态24小时平均血压升高≥10%，7例患者（19%）被归类为盐敏感型，30例患者（81%）为盐抵抗型。在盐敏感性测试前，当患者按习惯盐摄入量（160 mmol氯化钠/24小时）饮食时，在静息状态和自行车运动期间检查中枢血液动力学（动脉内压力、染料稀释法测定的心输出量、心电图测定的心率和总外周阻力）。尽管盐敏感组和盐抵抗组对一周高盐饮食的血压反应存在显著差异（27/9 mmHg对 -2/1 mmHg），但两组之间的任何中枢血液动力学变量均无差异。此外，两组之间在神经体液变量或左心室大小的超声心动图指标方面未观察到统计学上的显著差异。由于采用了有创血液动力学检查方法，在高盐或低盐摄入期间未再次研究中枢血液动力学。结论是，盐敏感型和盐抵抗型高血压患者在按习惯盐饮食时，中枢血液动力学无差异。
