Abolition of long-term vascular influence of renin-angiotensin system.
Abolition of long-term vascular influence of renin-angiotensin system.
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消除肾素-血管紧张素系统的长期血管影响。
DOI：
10.1152/ajpheart.1990.259.2.h543
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Zimmerman,BG
中科院分区：
文献类型：
--
作者：
Randall,RD;Zimmerman,BG
家兔双侧肾切除24小时或接受血管紧张素转换酶（ACE）抑制剂慢性（5天）前的急性实验。通过同时测量血压和髂动脉血流量，确定交感神经刺激（SNS）（0.25、0.75和2.25 Hz）和去甲肾上腺素（NE）给药（0.2、0.6和1.8 μ g ia）的电导反应。与正常对照组相比，肾切除组（44，26和20%）和慢性ACE抑制组（39，31和24%）对SNS的电导反应显著降低，而对NE的电导反应无变化。与正常对照组相比，持续输注血管紧张素II（ANG II）24 h可恢复肾切除组和慢性ACE抑制组对SNS的抑制反应，但不改变对NE的电导反应。与对照组相比，急性ACE抑制不影响对SNS或NE的电导反应。血管组织ACE活性在急性和慢性ACE抑制组抑制程度与正常兔相似（50%）。钠耗竭增加了对SNS的电导反应（0.25和0.75 Hz时分别为30%和24%），但对NE的反应不受影响。慢性ACE抑制显着减弱的电导反应SNS和轻微降低的反应去甲肾上腺素在钠耗尽的兔子。因此，在麻醉兔中，肾素-血管紧张素系统可能通过ANG II作用于连接前部位而增强SNS的作用，并且ANG II的这种作用似乎是长期的。因此，肾素-血管紧张素系统除了在病理生理状态下支持动脉压的能力之外，还在血压控制中发挥生理作用。
Rabbits were bilaterally nephrectomized for 24 h or received an angiotensin-converting enzyme (ACE) inhibitor chronically (5 days) before an acute experiment. Conductance responses to sympathetic nerve stimulation (SNS) (0.25, 0.75, and 2.25 Hz) and norepinephrine (NE) administration (0.2, 0.6, and 1.8 micrograms ia) were determined from simultaneous blood pressure and iliac blood flow measurements. Conductance responses to SNS were significantly reduced in nephrectomized (44, 26, and 20%) and chronic ACE inhibition (39, 31, and 24%) groups compared with normal controls, whereas conductance responses to NE were unchanged. Continuous infusion of angiotensin II (ANG II) for 24 h restored the depressed responses to SNS in nephrectomized and chronic ACE inhibition groups compared with normal controls but did not change conductance responses to NE. Acute ACE inhibition did not affect the conductance responses to SNS or NE compared with controls. Vascular tissue ACE activity was inhibited to a similar degree (50%) in both acute and chronic ACE inhibition groups compared with normal rabbits. Sodium depletion increased the conductance responses to SNS (30 and 24% at 0.25 and 0.75 Hz, respectively), but responses to NE were not affected. Chronic ACE inhibition significantly attenuated the conductance responses to SNS and slightly decreased responses to NE in sodium-depleted rabbits. Thus, in the anesthetized rabbit, the renin-angiotensin system potentiates the effect of SNS, presumably by ANG II acting at a prejunctional site, and this effect of ANG II appears to be long term in nature. Therefore, the renin-angiotensin system exerts a physiological role in the control of blood pressure in addition to the ability of this system to support arterial pressure in pathophysiological states.