ADRENERGIC DYSFUNCTION IN UREMIA

部分肾切除尿毒症大鼠提供了一种很好的模型 检查尿毒症对肾上腺素能神经系统的影响。用人 尿毒症大鼠肠系膜血管制剂及γ-1，选择性 放射性配基(125I)IBE2254，尿毒症对肾上腺素能效应的影响 全身血管阻力的组成部分；γ-1，血管受体， 将会被评估。需要检验的假设是慢性尿毒症导致 高血压的一种神经源性形式，类似于实验中观察到的 具有压力感受器差异的模型。在这样的模型中，补药的丧失 抑制交感神经血管运动流出，导致交感神经 介导血管收缩，增加儿茶酚胺的合成和 高血压。具体目标包括： 1)确定肾组织中γ1血管受体的数量是否减少 尿毒症大鼠。以内源性增加为特征的生理状态 儿茶酚胺的水平与伽玛的下调有关 1血管受体。通过测定血浆儿茶酚胺水平，我们将 能够将这些与观察到的受体数量的任何变化相关联。 2)确定Gamma 1血管受体的亲和力是否被钝化 或因尿毒症状态而降低。 在尿毒症大鼠身上也进行了一系列相关的研究 慢性尿毒症对心肌B细胞密度和亲和力的影响 肾上腺素能受体；和B受体；腺苷环化酶偶联，将 检查过了。

The partially nephrectomized uremic rat provides an excellent model to examine the effect of uremia on the adrenergic nervous system. Employing the uremic rat mesenteric vascular preparation, and the Gamma 1, selective radioligand (125I) IBE2254, the effect of uremia on the adrenergic effector component of systemic vascular resistance; the Gamma 1, vascular receptor, will be assessed. The hypothesis to be tested is chronic uremia results in a neurogenic form of hypertension, similar to that observed in experimental models with baroreceptor differentation. In such models, loss of tonic inhibition of sympathetic vasomotor outflow, results in sympathetically mediated vasoconstriction, increased catecholamine synthesis and hypertension. Specific objectives include: 1) To determine if the number of Gamma 1 vascular receptors is decreased in uremic rats. Physiologic states characterized by increased endogenous levels of catecholamines have been associated with down regulation of Gamma 1 vascular receptors. By determining plasma catecholamine levels, we will be able to correlate these with any changes in receptor number observed. 2) To determine if the affinity of the Gamma 1 vascular receptor is blunted or decreased by the uremic state. In a series of related investigations also performed in the uremic rat model, the effect of chronic uremia on density and affinity of myocardial B adrenergic receptors; and B receptor; adenyl cyclase coupling, will be examined.