Roles of neuropeptides in the neural control of cardiovascular function.

神经肽在心血管功能神经调控中的作用.在麻醉和清醒大鼠上，观察了刺激下丘脑室旁核（PVN）对动脉压、心率和肾交感神经活动（RSNA）的影响。PVN是神经肽影响自主神经功能的作用部位之一。在麻醉大鼠中，电流和L-谷氨酸刺激PVN降低RSNA伴随着动脉压的降低。另一方面，刺激PVN增加RSNA伴随着清醒大鼠动脉压的增加。结论：PVN神经元通过交感神经系统参与升压和降压控制系统，麻醉对这两个控制系统的平衡有重要影响.侧脑室注射神经肽对麻醉和清醒大鼠动脉压、心率和RSNA的影响 ...更多信息 .（一）.血管紧张素II（AII）的管理引起的动脉压升高和RSNA的剂量依赖性的方式减少。清醒大鼠心率下降，但麻醉大鼠没有显示任何变化。通过预先i. c. v.给药AII拮抗剂saralasin，反应大大减弱。AII诱导的RSNA减少持续存在于大鼠去窦弓神经，表明RSNA的减少不是由于压力感受器激活。此外，多普勒血流探头测量的肾血流量没有显着变化。因此，在i. c. v. AII之后观察到的rsna的减少可能涉及控制来自肾小管的肾素释放和/或钠和水的吸收，而不是肾血流动力学。（二）、心钠素（ANP）的管理没有改变动脉压，心率和RSNA。然而，ANP减弱AII诱导的升压和心动过缓反应，但不影响AII诱导的RSNA的抑制作用。因此，建议中心相互作用位点。AII和ANP对心血管和肾脏反应的影响可能不同。少

Roles of neuropeptides in the neural control of cardiovascular function.1. Effects of stimulation of the hypothalamic paraventricular nucleus (PVN), where is one of sites of action for the effects of neuropeptides on autonomic functions, were examined on arterial pressure, heart rate and renal sympathetic nerve activity (RSNA) in anesthetized and awake rats. In anesthetized rats, stimulation of the PVN with electrical current and L-glutamate decreased RSNA accompanied by decrease in arterial pressure. On the other hand, the stimulation of the PVN increased the RSNA accompanied by increase in arterial pressure in awake rats. Therefore, it is concluded that PVN neurons are involved in both pressore and depressor controlling system through the sympathetic nerve system, and anesthesia strogly affects the balance of the two controlling system.2. Effects of intracerebroventricular (i.c.v) administration of neuropeptides on arterial pressure, heart rate and RSNA in anesthetized and awake rats … More . (1). Administration of angiotensin II (AII) evoked an increase in arterial pressure and a decrease in RSNA in dose-dependent manner. Heart rate decreeased in awake rats but did not show any change in anesthetized rats. The responses were greatly attenuated by prior i.c.v. administration of AII antagonist, saralasin. The decrease in RSNA induced by i.c.v. AII persisted in rats with sinoaortic denervation, indicating that the decrease in RSNA is not due to baroreceptors activation. Furthermore, renal blood flow measured by Doppler flow probes did not change significantly. thus, the decrease in rsna observed following i.c.v. aii might be involved in the control of renin release and/or absorption of sodium and water from the renal tubulus, rather than renal hemodynamics. (2). Administration of atrial natriuretic hormone (ANP) did not change arterial pressure, heart rate and RSNA. However, ANP attenuated AII-induced pressor and bradycardia responses but did not affect AII-induced depressant effects on RSNA. Therefore, it is suggested that central interacting sites. of AII and ANP for cardiovascular and renal responses may be different. Less