Randall R D, Zimmerman B G
Department of Pharmacology, University of Minnesota, Minneapolis 55455.
Am J Physiol. 1990 Aug;259(2 Pt 2):H543-53. doi: 10.1152/ajpheart.1990.259.2.H543.
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.
在急性实验前，对兔子进行双侧肾切除24小时，或长期（5天）给予血管紧张素转换酶（ACE）抑制剂。通过同时测量血压和髂血流量，确定对交感神经刺激（SNS）（0.25、0.75和2.25赫兹）和去甲肾上腺素（NE）给药（0.2、0.6和1.8微克，腹腔注射）的电导反应。与正常对照组相比，肾切除组（分别为44%、26%和20%）和长期ACE抑制组（39%、31%和24%）对SNS的电导反应显著降低，而对NE的电导反应未改变。与正常对照组相比，肾切除组和长期ACE抑制组连续输注血管紧张素II（ANG II）24小时可恢复对SNS的抑制反应，但对NE的电导反应未改变。与对照组相比，急性ACE抑制不影响对SNS或NE的电导反应。与正常兔子相比，急性和慢性ACE抑制组的血管组织ACE活性均受到相似程度（50%）的抑制。缺钠增加了对SNS的电导反应（在0.25和0.75赫兹时分别增加30%和24%），但对NE的反应未受影响。在缺钠的兔子中，长期ACE抑制显著减弱了对SNS的电导反应，并略微降低了对NE的反应。因此，在麻醉的兔子中，肾素-血管紧张素系统增强了SNS的作用，推测是通过ANG II作用于节前部位，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血压的能力外，还在血压控制中发挥生理作用。
