ROLE OF NEUROPEPTIDE Y IN NEURAL CONTROL OF THE HEART

本研究项目的长期目标是获得更多的 完全理解神经肽Y在神经系统中的作用， 控制心脏。 丰富的神经肽Y储存共存 交感神经末梢中的去甲肾上腺素 心脏，交感神经激活引起伴随的释放 神经肽Y和去甲肾上腺素 的具体目标 建议的实验是（l）确定的影响， 神经肽Y对迷走神经诱导的心脏变时性，变力性， 和传导性反应，（2）以确定心脏如何 含有神经肽Y的交感神经元分布于 心脏的各种功能区域，和（3）调查 调节神经肽Y释放和清除的因子 发自内心的 我们将评估简短的抑制效果 交感神经刺激对迷走神经诱导的变时性， 变力性和传导性反应，在我们给药之前和之后， 肾上腺素能受体拮抗剂。 我们会监测迷走神经- 在单独刺激后诱导心脏反应，右侧 和左锁骨下袢，以确定 含神经肽Y的交感神经纤维到各种结构 的心脏。 我们会刺激心脏的交感神经， 将神经肽Y和去甲肾上腺素的溢出量 冠状窦血液，期间和之后的交感神经停止 刺激. 我们将把神经肽Y的溢出与 冠状静脉窦血与神经肽Y的作用 迷走神经诱导的心脏变时性反应。 我们将测量 冠状窦血浆去甲肾上腺素含量， 反相高效液相 色谱电化学检测，我们将测量 用特异性放射免疫测定法测定血浆中的含量。 我们 将决定迷走神经刺激和肾上腺素能受体 阻断调节交感神经肽Y的溢出 神经元的方式类似于调制的溢出， 去甲肾上腺素 我们将评估神经肽Y在 抑制交感神经释放去甲肾上腺素 在持续的心脏交感神经刺激期间的终端。 神经肽Y在神经调控中的作用 心脏的重要性在于神经肽Y的释放 与心脏交感神经的去甲肾上腺素一起 终端在生理条件下。 因此，神经肽Y是 可能在心脏的瞬间调节中发挥作用 自主神经系统的功能。

The long term objective of this research project is to gain a more complete understanding of the role of neuropeptide Y in the neural control of the heart. Abundant stores of neuropeptide Y coexist with norepinephrine in sympathetic nerve terminals throughout the heart, and sympathetic activation evokes the concomitant release of neuropeptide Y and norepinephrine. The specific aims of the proposed experiments are (l) to determine the effects of neuropeptide Y on vagally-induced cardiac chronotropic, inotropic, and dromotropic responses, (2) to determine how the cardiac sympathetic neurons that contain neuropeptide Y are distributed to various functional regions of the heart, and (3) to investigate the factors that modulate the release and removal of neuropeptide Y from the heart. We will assess the inhibitory effect of brief train of sympathetic stimulation on vagally-induced chronotropic, inotropic, and dromotropic responses, before an after we administer adrenergic receptor antagonists. We will monitor the vagally- induced cardiac responses after individually stimulating, the right and left ansae subclaviae, to determine the distribution of neuropeptide Y-containing sympathetic fibers to various structures of the heart. We will stimulate the cardiac sympathetic nerves and compare the overflows of neuropeptide Y and norepinephrine into the coronary sinus blood, during and after the cessation of sympathetic stimulation. We will correlate the overflow of neuropeptide Y in the coronary sinus blood with the effects of neuropeptide Y on vagally-induced cardiac chronotropic responses. We will measure the coronary sinus plasma content of norepinephrine by means of reverse-phase high performance liquid chromatography with electrochemical detection, and we will measure the plasma content of by means of specific radioimmunoassay. We will determine whether vagal stimulation and adrenergic receptor blockade modulate the overflow of neuropeptide Y from sympathetic neurons in a manner similar to the modulation of the overflow of norepinephrine. We will assess the role of neuropeptide Y in suppressing the release of norepinephrine from sympathetic nerve terminals during sustained cardiac sympathetic stimulation. Knowledge of the function of neuropeptide Y in the neural control of the heart is important because neuropeptide Y is released together with norepinephrine from cardiac sympathetic nerve terminals under physiologic conditions. Thus, neuropeptide Y is likely to play a role in the moment to moment regulation of cardiac function by the autonomic nervous system.