BLOOD PRESSURE REACTIVITY IN BLACKS--FUNCTION OF EXERCISE/FAMILIAL HYPERTENSION

非裔美国人的高血压发病率最高 比美国的任何种族群体都要多。造成这一高度的原因 艾滋病毒在这一人群中的流行率尚不清楚。有一个不可否认的 高血压的遗传成分；然而，这只占了 血压的变化导致许多研究人员强调 环境因素的额外重要性，如压力和身体状况 无所事事。研究表明，缺乏身体活动的人 高血压父母的后代对高血压的反应被夸大了 压力。英国石油公司对石油的响应异常增加的例子 血压正常的个体中的应激具有临床重要性，因为 这种加压反应与疾病的原因或标志有关。 高温超导技术的未来发展。BP反应性的异常增加 久坐不动的个人和高血压父母的子女的压力 归因于交感神经活性(SNA)的升高 改变心输出量和/或全身血管阻力。有氧 体力活动干预已被证明可以降低SNA，从而 可能会改变加压反应对压力的反应。是否有家族病史 高血压与体力活动的相互作用影响血压对应激的反应 非洲裔美国人并不为人所知。我们假设有氧运动 活动干预将减弱血压对应激的反应 久坐的血压正常的年轻成年非裔美国人，有家族性 热门歌曲的历史。我们进一步假设有氧体力活动将 减弱久坐不动的正常血压青年组的血压反应 有高血压家族史的非裔美国人(n=12名女性和12名 男性)，无高血压家族史(女性12例，男性12例) 将接受为期12周的有氧体育活动干预计划。 家族性高血压大小相近的久坐组(12名女性和12名男性) 没有家族性高血压(12名女性和12名男性)将不会经历 体力活动干预，并将作为对照。收缩压， 舒张压和平均动脉压在基线和 挑衅性精神和身体压力的条件将被确定 并对组间差异进行分析。心脏最大摄氧量 输出量、每搏输出量、全身血管阻力、心率、心脏 自主神经流出和骨骼肌血流量将被测量到 确定观察到的效应的可能机制(S)。的模式 观察到的反应将增加我们对 遗传学、体力活动干预和压力对精神分裂症的控制 血压，以及参与血压控制的心血管因素。

African Americans have the highest incidence of essential hypertension (HT) than any racial group in the United States. The cause of this high prevalence of HIV in this population is not known. There is an undeniable genetic component to HT; however, this account for only a portion of the variance in blood pressure (BP) leading many researchers to emphasize the additional importance of environmental factors such as stress and physical inactivity. Studies have indicated that physically inactive individuals and offspring of hypertensive parents have an exaggerated BP response to stress. Demonstrations of abnormal increases in BP responsiveness to stress among normotensive individuals is of clinical importance in that such pressor reactivity is associated with the cause of or a marker for future development of HT. This abnormal increase in BP reactivity to stress in both sedentary individuals and offspring of hypertensive parents is attributed to an elevated sympathetic neural activity (SNA) which alters the cardiac output and or systemic vascular resistance. Aerobic physical activity intervention has been shown to decrease the SNA and thus may alter the pressor reactivity to stress. Whether a familial history of HT interact with physical activity to affect BP responses to stress in African Americans is not known. We hypothesize that aerobic physical activity intervention will attenuate the BP response to stress in sedentary normotensive young adult African Americans with a familial history of HIT. We further hypothesize that aerobic physical activity will attenuate the BP response to groups of sedentary normotensive young adult African Americans with a familial history of HT (n= 12 females and 12 males) and without a familial history of HT (n= 12 females and 12 males) will undergo a 12 week aerobic physical activity intervention program. Similar size sedentary groups with familial HT (12 females and 12 males) and without familial HT (12 females and 12 males) will not undergo the physical activity intervention and will serve as the control. Systolic Bp, diastolic BP, and mean arterial BP responses at baseline and during conditions of provocative mental and physical stress will be determined and analyzed for between-group differences. Maximal oxygen uptake, cardiac output, stroke volume, systemic vascular resistance, heart rate, cardiac autonomic outflow, and skeletal muscle blood flow will be measured to determine the possible mechanism(s) of observed effects. The pattern of responses observed will increase our understanding of the interaction of genetics, physical activity interventions, and stress in the control of BP, and the cardiovascular factors involved in BP control.