ACUTE BARORECEPTOR RESETTING IN HYPERTENSION

动脉压力感受器在调节动脉压力中起主要作用。 急性心血管应激时的动脉血压， 出血和病理生理状态如高血压。 在动脉压升高期间动脉压力感受器的激活 压力引起交感神经活动的反射抑制， 缓冲动脉压的上升。 动脉水平 这些感受器的压力和它们对 因此，压力的变化是一个重要的决定因素 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”， 在更高的压力下点火并且它们的灵敏度降低， 导致动脉压持续升高 （慢性重置）。 这种重置现象也发生在 血压正常的动物在动脉暂时升高后 压力超过10-15分钟（急性重置）。 的 研究的目的是：（1）相对 压力感受器的急性重置程度， 无髓传入纤维; 2）可能的贡献 循环肽（血管紧张素II和加压素），以急性 动脉压力反射的重调定; 3） 交感神经流出对短暂变化的反应（10-15分钟）在 动脉压; 4）中枢神经系统对短暂 传入压力感受器输入的变化，以及5）差异 正常血压和高血压动物之间的任何 以上回答。 单个单位压力感受器放电将 记录在有髓和无髓传入纤维， 将检查对脉动压力的急性变化的反应。 传出交感神经活动将被记录和反射 将控制区域交感神经流出（腰和肾） 在主要压力发生短暂变化后进行评估。 在 为了评估循环肽对这些的贡献， 响应，实验将在以下情况下重复： 血管加压素和肾素-血管紧张素系统的阻断剂。 中央 机制将通过操纵中央 传入输入（传入神经的电刺激）和 观察对传出交感神经反射控制的影响 神经活动 血压正常和 高血压动物应该了解生理和 病理生理机制参与反射神经- 体液对血液循环的控制

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.