BLOOD PRESSURE EFFECTS OF BEHAVIORAL STRESS / SODIUM LOADING

这项研究考察了生理和心理因素 与血压正常的成年人的血压升高有关。这个 这项研究的长期目标是发展和完善 对高血压的预防性干预，无论是行为干预还是 饮食，这可以针对那些最 易受行为性高血压协同效应的影响 压力和高钠摄入量。约翰霍普金斯大学的医科学生 大学医学院参与了两个不同的部分 学习，一次在两周的考试期间，一次在 压力很大的实验室规程。42名医学生穿着 讲座期间和讲座期间的动态血压监测仪 维持高钠(N=28)和正常钠的同时检查 摄入(N=14)。参加考试的压力与 血浆钾降低，血浆皮质醇升高， 有升高血浆钠的趋势。不出所料，血压和 在考试过程中心率比讲座时加快 期间，但这些高程的大小不受 钠摄入量。收集定时尿样，并进行检查 与尿液排泄率的降低有关，尽管两者 尿皮质醇和尿去甲肾上腺素有增加的趋势 压力很大的考试。老年患者尿皮质醇排泄量 高钠组的检查更多，而尿液 高钠组去甲肾上腺素排泄量呈下降趋势。 尿钠排泄数据被用来确定 个人，包括钠固位体(减少48%的尿钠 考试期间的排泄率(UNA)和钠 排泄物(52%增加UNA)。钠固位体显示出更高的钠 控制(演讲)条件下的排泄率和较低的钠 暴露于应激源时的排泄率。这些人还 在应激前表现出较低的夜间钠排泄 考试。钠固位体显示出血液更多的趋势 对应激考试的压力反应性，有升高的趋势 检查过程中尿去甲肾上腺素排泄水平，以及 静息状态下30分钟内醛固酮水平升高的趋势 在考试之前。在第二项研究中，医学生(N=7)完成了 一项4.5小时的实验室方案旨在检查急性心血管疾病， 神经激素和肾脏对压力采访的反应。压力- 29%的样本观察到诱导性钠滞留。初步 结果表明，应激诱导的钠滞留与 血浆促肾上腺皮质激素和 Aidosterone水平，尽管两组显示出相似的血液 在压力重重的面试中，压力会上升。 观察到应激诱导的钠滞留持续到一个- 一小时恢复期。这些发现表明， 肾上腺皮质激活，特别是醛固酮刺激，在 对行为挑战的反应可能是压力的中介物- 相关的钠离子滞留。

This study examines the physiological and psychological factors associated with blood pressure elevations in normotensive adults. The long-term goal of this research is the development and refinement of preventative interventions for hypertension, either behavioral or dietary, that can be directed at those individuals who are most vulnerable to the synergistic blood pressure effects of behavioral stress and a high sodium intake. Medical students at Johns Hopkins University School of Medicine participated in two different parts of the study, once during the two-week examination period and once during a stressful laboratory protocol. Forty-two medical students wore ambulatory blood pressure monitors during a lecture and during the examination while maintaining the high sodium (N=28) and regular sodium intake (N=14). The stress of taking an examination was associated with a lowering of plasma potassium, an increase in plasma cortisol, and a tendency to increase plasma sodium. As expected, blood pressure and heart rate were elevated during the examination relative to the lecture period, but the magnitude of these elevations were not influenced by sodium intake. Timed urine samples were collected and the examination was associated with a reduction in urinary excretion rate, although both urinary cortisol and urinary norepinephrine tended to increase during the stressful examination. Urinary cortisol excretion during the examination was greater among the high sodium group, whereas urinary norepinephrine excretion tended to be lower in the high sodium group. Urinary sodium excretion data were used to identify subsets of individuals, including sodium retainers (48% decreased urinary sodium excretion rate (Una) during the exam relative to the lecture) and sodium excreters (52% increased Una). Sodium retainers showed higher sodium excretion rates during the control (lecture) conditions and lower sodium excretion rates during exposure to the stressor. These individuals also showed lower overnight sodium excretion before the stressful examination. Sodium retainers showed a tendency for greater blood pressure reactivity to the stressful examination, a tendency for higher levels of urinary norepinephrine excretion during the examination, and a tendency for higher resting levels of aldosterone collected 30 minutes before the exam. In a second study, medical students (N=7) completed a 4.5 hr laboratory protocol designed to examine acute cardiovascular, neurohormonal, and renal responses to a stressful interview. Stress- induced sodium retention was observed in 29% of the sample. Preliminary results indicate that stress-induced sodium retention was associated with higher levels of plasma adrenocroticotrophin hormone and aidosterone levels, although both groups showed comparable blood pressure elevations in response to the stressful interview. Stressinduced sodium retention was observed to continue into the one- hour recovery period. These findings suggest the importance of adrenocortical activation, particularly aldosterone stimulation, in response to behavioral challenges as a possible mediator of stress- related sodium retention.