MICROPUNCTURE STUDY OF KIDNEY FUNCTION

我们建议继续研究肾功能利用显微穿刺 和微灌注技术来测量肾小球和肾小管功能， 以及多单位和单单位神经记录，用于评估神经功能 控制肾功能。 年轻遗传学家的平行研究 Okamoto-Aoki品系高血压大鼠（SHR）和适当的对照组 将提供深入了解肾功能的作用及其调节， 在该模型中高血压发展的神经体液机制， 类似于人类的原发性高血压。 抑制 前列腺素合成减弱了对去神经支配的利钠反应; 肾单位网站的这种明显的许可行动的murlandins将 在急性和慢性失神经支配的肾脏中都可以识别。 的作用 三尖杉酯碱调节肾神经的抗利尿反应 刺激也将被调查，以及是否改变的问题， 基底神经活动和/或前列腺素合成受损 在某些品系的大鼠中缺乏去神经利钠作用， 在某些形式的麻醉后，将被解决。 的相对 各种类型的肾化学感受器的出现频率， 机械感受器，以及它们对生理刺激的反应，将被 测量年轻SHR和正常血压对照。 活动单 还将测量传出肾神经纤维，并且它们的反射 对R1和R2的化学感受器的激活的反应性 将评估桡神经中躯体传入神经的亚型和类型。 肾小管性肾小球反馈（TGF）在肾皮质自身调节中的作用 肾小球超滤和肾血流量将在 正常血压和遗传性高血压大鼠。 研究具体 旨在深入了解负责的机制， 年轻遗传性高血压患者TGF活性增强的后果 大鼠 TGF-β 1表达时持续自身调节的机制 受损的将被调查，和合成心房的影响 利钠因子对肾小球超滤动力学，节段性 将检查血管阻力和TGF。

We propose to continue studies of kidney function utilizing micropuncture and microperfusion techniques to measure glomerula and tubular function, and multiunit and single unit nerve recordings for assessment of neural control of renal function. Parallel studies in young genetically hypertensive rats of the Okamoto-Aoki strain (SHR) and appropriate controls will provide insight into the role of renal function and its regulation by neurohumoral mechanisms in the development of hypertension in this model, which resembles essential hypertension in humans. Inhibition of prostaglandin synthesis blunts the natriuretic response to denervation; the nephron sites of this apparently permissive action of prostaglandins will be identified in both acutely and chronically denervated kidneys. The role of prostaglandins in modulating the antinatriuretic response to renal nerve stimulation will also be investigated, and the question whether altered basal nerve activity and/or impaired prostaglandin synthesis is responsible for the absence of denervation natriuresis in certain strains of rats and after certain forms of anesthesia will be addressed. The relative frequency of occurence of various types of renal chemoreceptors and mechanoreceptors, and their responsiveness to physiologic stimuli, will be measured in young SHR and normotensive controls. The activity of single efferent renal nerve fibers will also be measured, and their reflex responsiveness to the activation of chemoreceptors of the R1 and R2 subtypes and of somatic afferents in the radial nerve will be assessed. The role of tubular glomerular feedback (TGF) in the autoregulation of glomerular ultrafiltration and renal blood flow will be investigated in normotensive and genetically hypertensive rats. Studies are specifically designed to gain insight into mechanisms responsible for, and functional consequences of, enhanced TGF activity in young genetically hypertensive rats. Mechanisms responsible for continued autoregulation when TGF is impaired will be investigated, and the effects of synthetic atrial natriuretic factor on glomerular ultrafiltration dynamics, segmental vascular resistance, and TGF will be examined.