MICROPUNCTURE STUDY OF KIDNEY FUNCTION

我们建议继续利用微穿刺法研究肾功能。 以及用于测量肾小球和肾小管功能的微灌注技术， 以及多单位和单单位神经记录用于神经评估 控制肾功能。青年遗传学的平行研究 Okamoto-Aoki品系高血压大鼠(SHR)及相应对照组 将提供对肾功能的作用及其调节的洞察力 神经体液机制在该模型高血压发病中的作用 这类似于人类的原发性高血压。抑制 前列腺素合成钝化去神经后的利钠反应； 这种明显允许前列腺素作用的肾单位部位将 在急性和慢性失神经的肾脏中均可发现。角色 前列腺素对肾神经抗心绞痛反应的调节作用 刺激也将被调查，以及是否改变了 基础神经活动和/或前列腺素合成受损是原因之一 在某些品系的大鼠中没有失神经的利钠作用 在某些形式的麻醉后，将解决。相对的 各种类型的肾脏化学感受器的出现频率和 机械感受器及其对生理刺激的反应将是 在年轻的自发性高血压患者和正常血压的对照组中测量。单人的活跃性 传出肾神经纤维也将被测量，它们的反射 对R1和R2化学受体激活的反应性 本课程将评估放射神经中躯体传入的亚型和类型。 肾小球小管反馈在肾小管上皮细胞自身调节中的作用 年将研究肾小球超滤和肾血流。 正常血压和遗传性高血压大鼠。研究特别是 旨在深入了解负责和运行的机制 年轻遗传性高血压患者转化生长因子活性增强的后果 老鼠。转化生长因子持续自我调节的机制 将对受损的人进行调查，并对人工心房的效果进行观察 尿钠因子对肾小球超滤动力学的影响 血管阻力和转化生长因子将被检测。

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.