Zimmerman J B, Robertson D, Jackson E K
J Clin Invest. 1987 Aug;80(2):443-57. doi: 10.1172/JCI113092.
This study tested the hypothesis that interactions of endogenous angiotensin II (AII) with the noradrenergic neuroeffector junction are important in renin-dependent hypertension. In the in situ blood-perfused rat mesentery, in normal rats exogenous AII potentiated mesenteric vascular responses to periarterial (sympathetic) nerve stimulation (PNS) more than vascular responses to exogenous norepinephrine (NE). In 2-kidney-1-clip (2K-1C) rats with renovascular hypertension mesenteric vascular responses to PNS and NE were greater than in sham-operated rats, and renovascular hypertension mimicked the effects of exogenous AII with respect to enhancing responses to PNS more than responses to NE. In 2K-1C rats, but not in sham-operated rats, 1-Sar-8-Ile-AII markedly suppressed vascular responses to PNS, without influencing responses to NE. Finally, 1-Sar-8-Ile-AII attenuated sympathetic nerve stimulation-induced neuronal spillover of NE in 2K-1C rats, but not in sham-operated rats. These data indicate that renovascular hypertension enhances noradrenergic neurotransmission, and that this enhancement is mediated in part by AII-induced facilitation of NE release.
内源性血管紧张素II（AII）与去甲肾上腺素能神经效应器接头的相互作用在肾素依赖性高血压中起重要作用。在原位血液灌注的大鼠肠系膜中，在正常大鼠中，外源性AII增强肠系膜血管对动脉周围（交感）神经刺激（PNS）的反应比增强对外源性去甲肾上腺素（NE）的反应更明显。在患有肾血管性高血压的2肾1夹（2K-1C）大鼠中，肠系膜血管对PNS和NE的反应比假手术大鼠更大，并且肾血管性高血压在增强对PNS的反应方面比增强对NE的反应方面模拟了外源性AII的作用。在2K-1C大鼠中，但在假手术大鼠中未出现，1- Sar-8- Ile-AII显著抑制血管对PNS的反应，而不影响对NE的反应。最后，1- Sar-8- Ile-AII减弱了2K-1C大鼠中交感神经刺激诱导的NE神经元溢出，但在假手术大鼠中未出现这种情况。这些数据表明，肾血管性高血压增强了去甲肾上腺素能神经传递，并且这种增强部分是由AII诱导的NE释放促进所介导的。
