RENAL AFFERENTS INVOLVED IN CARDIOVASCULAR REGULATION

传入肾神经（ARN）参与了动脉的控制， 压力、液体平衡和输尿管梗阻引起的剧烈疼痛。 电刺激ARN诱发反射对动脉血压的影响 和交感性高血压。 机械或化学刺激 激活特定的ARN纤维群， 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 本提案的目标是 确定特定模态ARN的脊柱和脊柱上投影 输入，这些神经元的中枢连接， 哪个ARN输入被调制以及ARN输入和 交感神经、血液动力学和行为活动。 大多数研究将需要识别单个 脊髓灰质神经元对ARN刺激的反应。 的关系 ARN输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自发活动 使用尖峰触发平均技术。 的结果 一项研究将确定ARN活动与交感神经活动的关系有多密切。 神经活动，以更好地定义肾内脏反射。 路径和 来自这些神经元的上行投射的终止场将是 由棘上部位的逆向激活细胞决定。 脊髓灰质细胞对特定化学和机械刺激的反应 还将确定肾的刺激以识别位点 对特定的刺激方式作出反应，并试图解释它们的 在脊髓和脊髓上反射中的作用。 紧张性下行调制 将通过比较之前对ARN刺激的反应来研究ARN输入。 颈髓冷阻滞后。 相位调制将 通过识别大脑中的部位进行检查， 刺激诱导的对ARN反应的促进或抑制 可以引发刺激。 附带调节和相互作用 还将研究压力感受器传入。 从这些 研究将阐明下降的程度、性质和来源， 调节影响，以阐明其在肾传入神经传导中的作用 输入. 最后，刺激ARN的血流动力学和行为学效应 将在清醒、自由活动的大鼠中观察，以确定 哪些ARN参与了动脉压、体液 平衡和内脏疼痛。 这些研究旨在阐明 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.