Ziegler M G, Lake C R
Fed Proc. 1984 Jan;43(1):62-6.
The study of patients with partial or total defects of their sympathetic nerves can help clarify the role of the sympathetic nervous system in blood pressure control. Denervation supersensitivity of both beta and alpha receptors develops in humans and is proportional to the degree of sympathetic withdrawal. Although alterations in beta-receptor sensitivity are familiar responses to beta agonists or antagonists, patients with decreased norepinephrine (NE) levels appear to develop alpha-receptor supersensitivity of greater hemodynamic importance. When beta supersensitivity is marked, there may be a pressor response to beta blockade even when circulating levels of NE and epinephrine are very low. Indomethacin blocks prostaglandin synthesis and causes an increase in blood pressure in patients with partial autonomic neuropathies. The drug increases blood pressure by enhancing alpha- and diminishing beta-receptor sensitivity to NE, so it is effective only in patients who have some residual NE release.
对交感神经部分或完全缺损患者的研究有助于阐明交感神经系统在血压控制中的作用。人类β受体和α受体均会出现去神经超敏反应，且与交感神经退缩程度成正比。虽然β受体敏感性改变是对β激动剂或拮抗剂的常见反应，但去甲肾上腺素（NE）水平降低的患者似乎会出现对血流动力学更重要的α受体超敏反应。当β超敏反应明显时，即使NE和肾上腺素的循环水平非常低，β受体阻滞剂也可能引起升压反应。吲哚美辛可阻断前列腺素合成，并导致部分自主神经病变患者血压升高。该药通过增强α受体敏感性和降低β受体对NE的敏感性来升高血压，因此仅对仍有一些NE释放的患者有效。
