BEHAVIOR FACTORS IN BLOOD PRESSURE REGULATION

之前对实验室动物的研究表明，尽管两者都不是 仅仅是厌恶的条件反射程序，或者单独的盐负荷增加了24%- HR平均血压，厌恶性条件反射和高 钠摄入量足以在体内产生实验性高血压 几天。本项目将这些发现扩展到对 人体血压的调节。 现在有两项研究表明，14天的高钠摄入量 准备考试的学生会增加静息血压(但 不是心率)，而无论是在以下情况下准备考试 正常的钠摄入量，或暑假期间的钠负荷，都没有 效果显著。伴随着这一人类模型的生理变化 实验性高血压已具有一定的特点。自发展以来 一项研究称，原发性高血压可能涉及自信行为的缺陷 已经开始评估心脏和呼吸系统的反应 血压正常和临界高血压的人到实验室的情况 模拟社交压力。这项研究还调查了培训的效果 放松对社交应激反应和动态血压的影响。 初步数据表明，高血压患者表现出更高水平的 PCO(2)高于实验室条件下的正常血压受试者。这 反应，如果是习惯性的，可以调节血压敏感度的增加 与高钠摄入量有关。

Previous studies with laboratory animals have shown that, although neither aversive conditioning procedures alone nor salt loading alone increased 24- hr mean blood pressure, a combination of aversive conditioning and high sodium intake were sufficient to engender experimental hypertension within days. The present project extends these findings to behavioral analysis of the regulation of human blood pressure. Two studies have now shown that 14 days of high sodium intake by medical students preparing for examinations increased resting blood pressure (but not heart rate), while neither preparation for examinations in a context of normal sodium intake, nor sodium loading during summer vacation, had any significant effect. Physiological changes accompanying this model of human experimental hypertension have been characterized. Since the development of primary hypertension may involve deficits in assertive behavior, a study has been initiated to assess cardio- respiratory responses of normotensive and borderline hypertensive humans to laboratory situations of simulated social stress. This study also investigates effects of training in relaxation on social stress reactivity and on ambulatory blood pressure. Preliminary data indicate that hypertensive subjects show higher levels of pCO(2) than normotensive subjects under laboratory conditions. This response, if habitual, could mediate increased blood pressure sensitivity to high sodium intake.