Anderson D E, Dhokalia A, Parsons D, Bagrov A Y
Laboratory of Cardiovascular Sciences National Institute on Aging/NIH, Baltimore, Maryland, USA.
J Hypertens. 1998 Jul;16(7):1015-22. doi: 10.1097/00004872-199816070-00016.
Previous research with normotensive adults aged over 40 years ('older') found that sensitivity of blood pressure of subjects with high resting end-tidal partial pressures of CO2 to high sodium intake was greater than normal.
To test the hypothesis that the lesser sensitivity of blood pressure of young normotensive adults to high sodium intake is also a function of resting end-tidal partial pressure of CO2.
Forty-eight Caucasian men and women (age 28.5 +/- 1.4 years) had a lower than normal dietary intake of sodium chloride for 4 days, and then ingested sodium chloride capsules for 7 days (an additional 190 mmol/day sodium chloride). Resting end-tidal partial pressure of CO2 and blood pressure, and 24 h ambulatory blood pressure, were measured before and after the high-sodium diet. Overnight urine samples were collected before and after the high-sodium diet to determine dietary compliance, and to assess changes in urinary excretion of endogenous digitalis-like factors (a ouabain-like factor, and a marinobufagenin-like factor) that covary with plasma volume.
Subjects with high end-tidal partial pressures of CO2 had lower resting heart rates and lower urinary excretion of ouabain-like factor before sodium loading. Sodium loading decreased mean partial pressure of CO2 (by 0.8 +/- 0.2 mmHg) and increased only ambulatory systolic blood pressure (by 2.1 +/- 0.8 mmHg) for the whole group. However, the changes in resting systolic (r = 0.32, P < 0.025) and diastolic (r = 0.36, P < 0.01) blood pressures and in 24 h systolic (r = 0.28, P < 0.05) blood pressure after sodium loading were all positive functions of individual resting end-tidal partial pressures of CO2. Sodium loading increased urinary excretion of marinobufagenin-like factor (by 1.78 +/- 0.88 nmol) and the magnitude of the individual increase was a function of end-tidal partial pressure of CO2.
The results indicate that a high resting partial pressure of CO2 augments the effects of high sodium intake on plasma volume, levels of endogenous digitalis-like factors, and blood pressure in young normotensive humans.
先前针对40岁以上(“年长”)血压正常成年人的研究发现,静息呼气末二氧化碳分压较高的受试者对高钠摄入的血压敏感性高于正常水平。
检验年轻血压正常成年人对高钠摄入的血压敏感性较低也是静息呼气末二氧化碳分压的一种作用这一假设。
48名白种男性和女性(年龄28.5±1.4岁)连续4天摄入低于正常水平的氯化钠饮食,然后连续7天服用氯化钠胶囊(额外每天摄入190 mmol氯化钠)。在高钠饮食前后测量静息呼气末二氧化碳分压和血压,以及24小时动态血压。在高钠饮食前后采集过夜尿液样本,以确定饮食依从性,并评估与血浆容量相关的内源性洋地黄样因子(一种哇巴因样因子和一种海蟾蜍精样因子)尿排泄量的变化。
静息呼气末二氧化碳分压较高的受试者在钠负荷前静息心率较低,哇巴因样因子尿排泄量较低。钠负荷使整个组的平均二氧化碳分压降低(降低0.8±0.2 mmHg),仅使动态收缩压升高(升高2.1±0.8 mmHg)。然而,钠负荷后静息收缩压(r = 0.32,P < 0.025)和舒张压(r = 0.36,P < 0.01)以及24小时收缩压(r = 0.28,P < 0.05)的变化均为个体静息呼气末二氧化碳分压的正函数。钠负荷增加了海蟾蜍精样因子的尿排泄量(增加1.78±0.88 nmol),个体增加幅度是呼气末二氧化碳分压的函数。
结果表明,高静息二氧化碳分压增强了高钠摄入对年轻血压正常人群血浆容量、内源性洋地黄样因子水平和血压的影响。