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1。刺激下丘脑室旁核(PVN)是神经肽影响自主神经功能的部位之一，本文观察了刺激下丘脑室旁核(PVN)对麻醉和清醒大鼠动脉压、心率和肾交感神经活动(RSNA)的影响。在麻醉大鼠，电刺激室旁核和L-谷氨酸可使RSNA降低，并伴有动脉压下降。另一方面，刺激PVN可增加清醒大鼠的RSNA，并伴有动脉压升高。结论：1.室旁核神经元通过交感神经系统参与升压和降压控制系统，麻醉严重影响这两个控制系统的平衡。侧脑室注射神经肽对麻醉和清醒…大鼠动脉压、心率和呼吸频率的影响更多。(1)。血管紧张素II(AII)以剂量依赖的方式引起动脉压升高和RSNA降低。清醒大鼠的心率减慢，但麻醉大鼠的心率没有任何变化。这些反应被先前的静脉注射大大减弱了。给药所有的拮抗剂，沙拉拉辛。静脉注射引起的RSNA下降。AII在去窦弓神经的大鼠中持续存在，表明RSNA的降低不是由于压力感受器的激活。此外，多普勒血流探头测得的肾血流量没有明显变化。因此，观察到静脉注射后RSNA的下降。AII可能参与控制肾素的释放和/或从肾小管吸收钠和水，而不是参与肾血流动力学。(2)。心房利钠激素(ANP)不改变动脉压、心率和RSNA。然而，ANP减弱了AII诱导的升压和心动过缓反应，但不影响AII诱导的抑制RSNA的作用。因此，建议中枢相互作用部位。AII和ANP对心血管和肾脏反应的影响可能不同。较少

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