AUTONOMIC FUNCTION IN RENOVASCULAR HYPERTENSION

描述：（改编自应用程序）：脑啡肽抑制释放 自主神经递质，从而减少对神经刺激的反应。 例如，脑啡肽减少迷走神经介导的心动过缓。 相反地， 肾上腺素能刺激心肌细胞导致脑啡肽增加 生产 肾上腺素能刺激增加见于高血压。 这 导致研究人员推测心脏反应性的降低 迷走神经刺激在高血压中看到可能与心脏 阿片肽 事实上，初步数据显示， 和儿茶酚胺含量的变化。 调查人员 假设1）高血压引起交感神经活动增加 减少脑啡肽降解，导致心脏脑啡肽增加; 脑啡肽增加导致自主神经反应性降低 刺激和增加心脏儿茶酚胺含量由于减少 心脏儿茶酚胺释放 实验将在体内进行， 慢性仪器高血压和对照犬，有和没有 β-肾上腺素能受体阻滞剂。 心脏脑啡肽降解活性 将在体外进行测量。 这些实验旨在回答： 交感神经活动增加导致脑啡肽增加 心脏脑啡肽在体内释放吗？ 阿片类药物是否抑制心脏 对自主神经刺激的反应 高血压会改变心脏吗 脑啡肽原加工还是脑啡肽降解？ 1)压力反射 在开发前和开发期间，将在有意识的犬中进行激发 肾血管性高血压或假手术。 动脉减少 硝普钠加压刺激交感神经，抑制迷走神经 外流。 苯肾上腺素升高动脉压抑制交感神经 刺激迷走神经流出 血浆心啡肽和儿茶酚胺 将测量溢出和心血管功能。 此外，本发明还提供了一种方法， 溢出和心脏功能将通过直接刺激 麻醉动物的迷走神经和交感神经 收藏在所有的组。 2)阿片肽对压力感受性反射的影响 功能将通过在存在的情况下重复压力反射激发来测试。 非选择性阿片受体拮抗剂二丙诺啡 第三章 组织脑啡肽酶活性、脑啡肽原产物和 将测定高血压动物与假手术对照动物中的儿茶酚胺含量。 心脏特异性将通过检查其他组织（肾上腺 腺、肾、肺、骨骼肌）。 高血压仍然是一个严重的 心血管疾病。 建议结果 将推进知识，并可能改善阿片类药物的治疗用途， 心脏病患者。

DESCRIPTION: (Adapted from the application): Enkephalins inhibit release of autonomic transmitters, thus, decreasing responses to nerve stimulation. For instance, enkephalins reduce vagally-mediated bradycardia. Conversely, adrenergic stimulation to cardiomyocytes causes increased enkephalin production. Increased adrenergic stimulation is seen in hypertension. This led the investigators to speculate that the decreased cardiac responsiveness to vagal nerve stimulation seen in hypertension may be linked to cardiac opioid peptides. Indeed, preliminary data show increased cardiac enkephalin and catecholamine content in hypertensive dogs. The investigators hypothesize that 1) hypertension-induced increases in sympathetic activity decrease enkephalin degradation leading to increased cardiac enkephalins; and 2) increased enkephalins cause decreased responsiveness to autonomic stimulation and increased cardiac catecholamine content due to decreased cardiac catecholamine release. Experiments will be conducted in vivo with chronically instrumented hypertensive and control dogs with and without beta-adrenergic receptor blockade. Cardiac enkephalin degrading activity will be measured in vitro. The experiments are designed to answer: Are increases in sympathetic activity responsible for increased enkephalins? Are cardiac enkephalins released in vivo? Do opioids depress cardiac responses to autonomic stimulation? Does hypertension change cardiac proenkephalin processing or enkephalin degradation? 1) Baroreflex challenges will be performed in conscious dogs before and during development of renovascular hypertension or the sham procedure. Decreased arterial pressure by nitroprusside stimulates sympathetic and depresses vagal outflows. Increased arterial pressure by phenylephrine inhibits sympathetic and stimulates vagal outflows. Cardiac enkephalin and catecholamine plasma spillover and cardiovascular function will be measured. In addition, spillover and cardiac function will be measured with direct stimulation of the vagus and sympathetic nerves in anesthetized animals before tissue collection in all groups. 2) Opioid peptide influence on baroreflex function will be tested by repeating baroreflex challenges in the presence of the non-selective opioid receptor antagonist, diprenorphine. 3) Measurement of tissue enkephalinase activity, proenkephalin products and catecholamine content in hypertensive vs. sham control animals will be made. Cardiac specificity will be determined by examining other tissues (adrenal gland, kidney, lung, skeletal muscle). Hypertension remains a serious cardiovascular problem in the population. It is suggested that the results will advance knowledge and may improve therapeutic use of opiates in patients with cardiac pathology.