Vollmer R R, Meyers S A, Ertel R J, Murthy V S
Clin Exp Hypertens A. 1984;6(5):993-1009. doi: 10.3109/10641968409044052.
Experiments were conducted in pithed Wistar rats to assess the effects of nephrectomy on the responsiveness of the cardiovascular system to sympathetic neurohumoral stimuli. Blood pressure and heart rate increases produced in response to stimulation of the spinal sympathetic outflow and to norepinephrine were compared in nephrectomized (NXR) and sham operated animals (SOR). Both the blood pressure (BP) and heart rate (HR) increases to nerve stimulation were markedly attenuated in the NXR, however, only the reduction in BP responses could be attributed to the absence of a functional renin angiotensin system. Infusion of angiotensin II (10 ng/kg/min) in NXR enhanced the neurally mediated increments in BP to the extent that the responses were not different from SOR. Angiotensin II administration also enhanced BP responses in SOR but to a lesser extent than in NXR. HR responses were not altered by angiotensin in NXR or SOR. Blockade of the renin angiotensin system in SOR with the converting enzyme inhibitor, captopril, reduced BP responses to the same level as NXR. In contrast, HR increments were not altered by captopril. BP but not HR increments to norepinephrine were significantly reduced in NXR. Infusion of angiotensin II restored the BP responses to a level equal to SOR; HR responses were not affected. In addition, captopril reduced the norepinephrine responses of SOR but not NXR. Thus the results of the present study indicate that endogenously formed angiotensin facilitates sympathetically mediated vasoconstrictor activity but does not influence heart rate responses. Therefore, the attenuation of neurally elicited increases in HR observed in NXR does not appear to be acutely related to reduced levels of angiotensin II.
在去大脑的Wistar大鼠身上进行实验，以评估肾切除对心血管系统对交感神经体液刺激反应性的影响。比较了肾切除（NXR）和假手术动物（SOR）对脊髓交感神经传出刺激和去甲肾上腺素刺激产生的血压和心率升高情况。NXR中对神经刺激的血压（BP）和心率（HR）升高均明显减弱，然而，只有BP反应的降低可归因于功能性肾素-血管紧张素系统的缺失。在NXR中输注血管紧张素II（10 ng/kg/min）可增强神经介导的BP升高，以至于其反应与SOR无差异。血管紧张素II给药也增强了SOR中的BP反应，但程度小于NXR。NXR或SOR中的血管紧张素均未改变HR反应。用转化酶抑制剂卡托普利阻断SOR中的肾素-血管紧张素系统，可将BP反应降低到与NXR相同的水平。相比之下，卡托普利未改变HR升高。NXR中对去甲肾上腺素的BP升高但不是HR升高明显降低。输注血管紧张素II可将BP反应恢复到与SOR相等的水平；HR反应未受影响。此外，卡托普利降低了SOR的去甲肾上腺素反应，但未降低NXR的反应。因此，本研究结果表明，内源性生成的血管紧张素促进交感神经介导的血管收缩活性，但不影响心率反应。因此，在NXR中观察到的神经引起的HR升高减弱似乎与血管紧张素II水平降低无急性关系。
