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

非裔美国人原发性高血压的发病率最高 (HT)比美国任何一个种族都多造成这种高度的原因 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 遗传成分HT;然而，这只占一部分， 血压（BP）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 不活动。研究表明，不运动的人 而高血压父母的后代对高血压的反应会更大， 应力血压对以下物质的反应性异常升高的证据 正常血压个体中的应激具有临床重要性， 这种升压反应性与以下疾病的原因或标志物有关 HT的未来发展。这种血压反应性的异常增加， 久坐者和高血压父母后代压力 这是由于交感神经活动（SNA）升高， 改变心输出量和/或全身血管阻力。有氧 体育活动干预已被证明会降低SNA， 可能会改变对压力的升压反应。是否有家族史 HT与体力活动相互作用影响血压对应激的反应， 美国人不知道。我们假设有氧运动 活动干预将减弱血压对压力的反应， 久坐不动的血压正常的年轻成年非洲裔美国人， HIT的历史我们进一步假设，有氧体育活动将 降低血压对久坐血压正常的年轻人的血压反应 有HT家族史的非裔美国人（n= 12名女性和12名 男性）和无HT家族史（n= 12名女性和12名男性） 将接受为期12周的有氧体育活动干预计划。 家族性HT患者的久坐组规模相似（12名女性和12名男性） 没有家族性HT（12名女性和12名男性）的患者将不接受 身体活动干预，并将作为对照。收缩压， 舒张压和平均动脉压反应，在基线和 挑衅性的精神和身体压力的条件将被确定 并分析组间差异。最大摄氧量，心脏 输出量、每搏输出量、全身血管阻力、心率、心脏 将测量自主流出和骨骼肌血流量， 确定观察到的效应的可能机制。的格局 观察到的反应将增加我们对以下因素相互作用的理解： 遗传学、身体活动干预和压力控制 血压，以及与血压控制有关的心血管因素。

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.