RENAL GLOMERULAR HEMODYNAMICS--NEURAL CONTROL MECHANISM

这项研究的长期目标是阐明其机制。 调节和调节肾血管(肾小球前和 肾小球后)对神经活动增加的反应。《解释》 正常的控制机制将有助于识别 与肾神经活性升高相关的病理情况 肾功能丧失(高血压)。拟议的研究将解决 以下概念：1)肾神经活动增加 不同的神经活动，诱发特定血管的收缩 去甲肾上腺素单独或与血管紧张素II联合应用，(3) 不同的α-1肾上腺素能受体亚型介导去甲肾上腺素 不同类型肾动脉狭窄和(4)大动脉狭窄 而小动脉对神经的刺激是由钙离子介导的 来自不同的来源(胞外和胞内)。这些 概念将通过观察活体肾脏微循环来解决。 大鼠肾积水的肾脏。肾小球前血管的直径， 肾小球被膜和毛细血管，以及传出小动脉 直接从校准的电视监视器直接测量 刺激肾神经(以不同的频率或持续时间)或 在反射引起的肾神经活动增加期间。刺激- 将为每个血管部位生成响应曲线以进行比较 相对血管反应性。肾小球血流动力学改变将是 通过直接测量肾小球毛细血管压力(伺服- 零系统)和血流(光学多普勒RBC流速仪)。要确定 去甲肾上腺素在选择性血管收缩中的作用 受体，刺激-反应曲线将在阻断后重复 α1a或α1b肾上腺素能受体。类似地， 循环血管紧张素II受体阻断。刺激的转变 反应曲线激动剂引起选择性收缩。衰减 钙通道阻滞剂的收缩反应将反映这种依赖性 不同血管对细胞外或细胞内钙内流的影响 钙释放对神经刺激的收缩作用。

The long-term objective of the research is to elucidate the mechanisms which mediate and regulate renal vascular (preglomerular and postglomerular) responses to increase in neural activity. The elucidation of normal control mechanisms will help to identify altered mechanisms in pathological conditions associated with elevated renal nerve activity and loss of kidney function (hypertension). The proposed research will address the following concepts: 1) Increases in renal nerve activity differentially nerve activity , constriction of specific vessels is induced by norepinephrine, alone or in combination with angiotensin II, (3) Different alpha-1 adrenergic receptor subtypes mediate norepinephrine constriction of different renal and (4) Constriction of large arteries versus small arterioles to nerve stimulation is mediated by calcium derived from different sources (extracellular versus intracellular). These concepts will be addressed by observing the in vivo renal microcirculation of the rat hydronephrotic kidney. The diameters of preglomerular vessels, glomerular capsules and capillaries, and efferent arterioles will be measured directly from a calibrated television monitor during direct stimulation of the renal nerve (at varing frequencies or duration) or during reflex-induced increase in renal nerve activity. Stimulation- response curves will be generated for each vascular site to compare relative vessel reactivity. Glomerular hemodynamic changes will be assessed by direct measurements of glomerular capillary pressure (servo- null system)and blood flow (optical doppler RBC velocimeter). To determine the role of norepinephrine to constrict select vessels via specific receptors, stimulation-response curves will repeated after blockade of alpha-la or alpha-1b adrenergic receptors. Similarly, the role of circulating angiotensin II receptor blockade. Shifts in the stimulation responses curves agonist to cause selective constriction. Attenuation of constrictor responses by calcium entry blockers will reflect the dependency of different vessels on influx of extracellular calcium or intracellular calcium release for constriction to nerve stimulation.