RENAL AFFERENTS INVOLVED IN CARDIOVASCULAR REGULATION

肾传入神经(ARN)参与动脉的控制。 压力、液体平衡和输尿管梗阻引起的剧烈疼痛。 电刺激ARN引起动脉压反射性改变 和大鼠交感高血压。机械或化学刺激 激活ARN纤维的特定群体，并相应地改变 传出交感神经活动。ARN输入的机制 对自主神经功能的影响尚不清楚。这项提议的目标是 确定特定通道ARN的脊髓和棘上投射 输入，这些神经元的中枢连接，性质和程度 哪个ARN输入被调制以及ARN输入和 交感神经、血流动力学和行为活动。 大多数研究将需要识别单一的 脊髓灰质神经元对ARN刺激有反应。两国关系 ARN传入和交感神经活动之间的关系将通过比较 这些神经元对内脏神经放电的自发活动 使用尖峰触发平均技术。这样做的结果 研究将确定ARN活动与交感神经的关系有多密切 神经活动，以更好地定义肾内脏反射。这条路和 来自这些神经元的上升投影的终止场将是 由反向激活脊椎上部位的细胞决定的。 脊髓灰质细胞对特定化学物质和机械作用的反应 还将确定肾脏的刺激部位 回应特定的刺激模式，并试图解释他们的 在脊椎和棘上反射中的作用。主音下行调制 将通过比较之前对ARN刺激的反应来研究ARN输入 颈髓冷凝后。相位调制将 通过识别大脑中的 刺激诱导的ARN反应的易化或抑制 刺激可以被引出。间接调节和相互作用 压力感受器传入也将被调查。来自这些的结果 研究将阐明下降的程度、性质和来源 阐明它们在肾传入神经传导中的调节作用 输入。最后，ARN刺激对血流动力学和行为的影响 将在清醒的、自由活动的大鼠中观察以确定程度 哪些ARN参与动脉压、体液的调节 平衡和内脏疼痛。这些研究旨在澄清 ARN的功能和解剖投影，以便更好地了解 它们在正常和病理状态下的作用。

Afferent renal nerves (ARN) have been implicated in the control of arterial pressure, fluid balance and the intense pain due to ureteral obstruction. Electrical stimulation of ARN elicits reflex changes in arterial pressure and sympathetic hypertension in rats. Mechanical or chemical stimuli activate specific populations of ARN fibers with corresponding changes in efferent sympathetic nerve activity. The mechanisms by which ARN input affects autonomic function are unknown. The goals of this proposal are to determine the spinal and supraspinal projections of modality-specific ARN input, the central connections of these neurons, the nature and extent to which ARN input is modulated and the relationship between ARN input and sympathetic, hemodynamic and behavioral activity. The majority of the studies will require the identification of single spinal gray neurons responding to ARN stimulation. The relationship between ARN input and sympathetic nerve activity will be done by comparing the spontaneous activity of these neurons to splanchnic nerve discharge using the technique of spike-triggered averaging. The results of this study will identify how closely ARN activity is coupled to sympathetic nerve activity to better define reno-visceral reflexes. The pathway and termination fields of ascending projections from these neurons will be determined by antidromically activating cells from supraspinal sites. Responses of spinal gray cells to specific chemical and mechanical stimulation of the kidney will also be determined to identify sites responsive to specific stimulus modalities and to try to interpret their role in spinal and supraspinal reflexes. Tonic descending modulation of ARN input will be studied by comparing responses to ARN stimulation before and after cold block of the cervical spinal cord. Phasic modulation will be examined by identifying sites in the brain from which stimulation-induced facilitation or inhibition of responses to ARN stimulation can be elicited. Collateral modulation and interactions with baroreceptor afferents will also be investigated. Results from these studies will elucidate the extent, nature and sources of descending modulatory influences to clarify their role in conduction of renal afferent input. Finally, the hemodynamic and behavioral effects of ARN stimulation will be observed in awake, freely moving rats to determine the extent to which ARN are involved in the regulation of arterial pressure, fluid balance and visceral pain. These studies are designed to clarify the functional and anatomical projections of ARN in order to better understand their role in normal and pathological states.