ACUTE BARORECEPTOR RESETTING IN HYPERTENSION

动脉压力感受器在血管紧张素转换酶的调节中起重要作用 急性心血管应激反应中的动脉血压 出血和病理生理状态，如高血压。 动脉血压升高时动脉压力感受器的激活 压力引起交感神经活动的反射性抑制 缓冲动脉压的升高。动脉水平 这些感受器将发射的压力及其对 因此，压力变化是一个重要的决定因素 对动脉压的神经调节。例如，在 在高血压状态下，这些压力感受器被“重置”，因此它们 在更高的压力下开火，它们的敏感度会降低， 有助于动脉血压的持续升高 (慢性重置)。这种重置现象也发生在 动脉短暂抬高后血压正常的动物 压力持续10-15分钟(急性重置)。这个 拟议研究的目的是检查：1)亲属 有髓鞘压力感受器急性重置的程度 无髓鞘传入纤维；2)可能的作用 循环肽(血管紧张素II和加压素)对急性 动脉压力反射的重置；3)区域差异 交感神经流出对短暂变化的反应(10-15分钟)在……里面 动脉压；4)中枢神经系统对短时间 传入压力感受器输入的变化，以及5)差异 血压正常的动物和高血压动物之间的关系 以上回应。单个单位的压力感应器排放将是 在有髓和无髓传入纤维中均有记录 本课程将研究脉动压剧烈变化时的反应。 传出的交感神经活动将被记录和反射 将控制区域交感神经流出(腰部和肾脏) 在当时的压力发生短暂变化后进行评估。在……里面 为了评估循环多肽对这些因素的贡献 响应时，实验将在有 加压素和肾素-血管紧张素系统的阻滞剂。中环 机制将通过操纵中央 传入输入(电刺激传入神经)和 传出交感神经对反射控制作用的观察 神经活动。正常血压和正常血压下的反应比较 高血压动物应该能够洞察到生理学和 反射神经参与的病理生理机制- 对循环的体液控制。

The arterial baroreceptors play a major role in the regulation of arterial blood pressure in acute cardiovascular stresses such as hemorrhage and in pathophysiologic states such as hypertension. Activation of the arterial baroreceptors during a rise in arterial pressure provokes a reflex inhibition of sympathetic activity and a buffering of the rise in arterial pressure. The level of arterial pressure at which these receptors will fire and their sensitivity to changes in pressure is therefore an important determinant of the neural regulation of arterial pressure. For example, in hypertensive states, these baroreceptors are "reset" so that they fire at a higher pressure and their sensitivity is reduced, contributing to the sustained elevation of arterial pressure (chronic resetting). This phenomenon of resetting also occurs in normotensive animals following temporary elevations of arterial pressure over a period of 10-15 minutes (acute resetting). The purpose of the proposed studies is to examine: 1) the relative degree of acute resetting of baroreceptors with myelinated and unmyelinated afferent fibers; 2) the possible contribution of circulating peptides (angiotensin II and vasopressin) to acute resetting of aterial baroreflexes; 3) regional differences in sympathetic outflow in response to brief changes (10-15 min.) in arterial pressure; 4) the central nervous system response to brief changes in afferent baroreceptor input, and 5) differences between normotensive and hypertensive animals in any of the above responses. Single unit baroreceptor discharge will be recorded in both myelinated and unmyelinated afferent fibers and responses to acute changes in pulsatile pressure will be examined. Efferent sympathetic nerve activity will be recorded and reflex control of regional sympathetic outflow (lumbar & renal) will be assessed following brief alterations in the prevailing pressure. In order to assess the contribution of circulating peptides to these responses, the experiments will be repeated in the presence of blockers of vasopressin and the renin-angiotensin system. Central mechanisms will be examined by manipulating the central afferent input (electrical stimulation of afferent nerves) and observing the effects on reflex control of efferent sympathetic nerve activity. Comparison of responses in normotensive and hypertensive animals should yield insight into both physiologic and pathophysiologic mechanisms involved in the reflex neural- humoral control of the circulation.