BLOOD PRESSURE EFECTS OF BEHAVIORAL STRESS AND SODIUM

高血压是心血管疾病的主要危险因素 脑血管疾病。动物实验室的证据表明 行为压力加上高钠摄入量可能会导致 对紧张性血压水平的协同作用及其原因 高血压。理解生理机制和识别 与这种监管缺失相关的心理特征 对血压的控制可能会导致开发和完善 对高血压进行有效的预防干预，无论是饮食 或行为上的，针对那些最 易受行为应激的血压协同效应影响 和高钠摄入量。 第一项研究将检查神经内分泌和其他调节 对高钠摄入量的反应(如血浆电解质的变化) 在应激性事件发生前的一段时间内给药(氯化钠x 压力)。医科学生将被给予补充钠 氯化物(600毫克/4.5公斤/天)或安慰剂片，采用双盲法 考试前14天内的方法(高压力)和 在学业要求低(压力小)的时期。心血管疾病， 神经内分泌和情绪变量将在休息时进行测量(高 和低压力)以及对考试的响应(仅限高压力)。 预计垂体肾上腺皮质系统的激活 将在调节nacl x应激血液中发挥更重要的作用。 压力升高比交感神经系统的激活和 更大的心血管、神经内分泌和情绪反应 这项检查表明，更大的压力将与 更大的氯化钠x应激血压反应。第二项研究将 确定血压和神经内分泌对实验室应激源的反应 人格因素，如敌意和压抑的愤怒，是 与较大的氯化钠x应激BP反应有关。在The High之前 应激性钠负荷期与心血管和神经内分泌反应 心算、社交挑战和与考试相关的学习 材料将被测量。预计压抑的愤怒和 对实验室应激源的更大的CV和神经内分泌反应 与更大的氯化钠x应激血压反应有关。第三 研究将确定同时摄入高钾是否会减少 氯化钠x胁迫的升压效应。主题将是 随机分配接受补钾氯化钠 平板电脑。预计并发的高钾摄入量将 钝化对氯化钠x应激血压的反应。

High blood pressure is a major risk factor for cardiovascular and cerebrovascular disease. Evidence from the animal laboratory indicates that behavioral stress combined with a high sodium intake can have synergistic effects on tonic blood pressure levels and cause hypertension. Understanding the physiological mechanisms and identifying the psychological characteristics associated with this loss of regulatory control over blood pressure could lead to the development and refinement of effective preventative interventions for hypertension, either dietary or behavioral, that are directed at those individuals who are most vulnerable to the synergistic blood pressure effects of behavioral stress and high sodium intake. The first study will examine neuroendocrine and other regulatory responses (e.g., changes in plasma electrolytes) to high sodium intake administered during the period preceding a stressful event (NaCl x STRESS). Medical students will be administered supplemental sodium chloride (600 mg/4.5 kg/day) or placebo tablets using a double-blind method during the 14 days prior to an examination (High Stress) and during a period of low academic demands (Low Stress). Cardiovascular, neuroendocrine, and emotional variables will be measured at rest (High and Low Stress) and in response to the examination (High Stress only). It is expected that activation of the pituitary adrenocortical system will play a more important role in mediating the NaCl x STRESS blood pressure elevations than activation of the sympathetic nervous system and that larger cardiovascular, neuroendocrine, and emotional responses to the examination, suggesting greater stress, will be associated with larger NaCl x STRESS blood pressure responses. The second study will determine whether BP and neuroendocrine responses to laboratory stressors and personality factors, such as hostility and suppressed anger, are associated with a larger NaCl x STRESS BP response. Prior to the High Stress sodium loading period, cardiovascular and neuroendocrine responses to mental arithmetic, social challenge, and studying exam-related material will be measured. It is expected that suppressed anger and greater CV and neuroendocrine reactivity to laboratory stressors will be associated with larger NaCl x STRESS blood pressure responses. The third study will determine whether a concurrent high potassium intake reduces the blood pressure elevating effects of NaCl x STRESS. Subjects will be randomly assigned to receive potassium supplemental sodium chloride tablets. It is expected that the concurrent high potassium intake will blunt the NaCl x STRESS blood pressure response.