Webb D J, Benjamin N, Cockcroft J R, Collier J G
Department of Clinical Pharmacology, St. George's Hospital Medical School, London, UK.
Am J Hypertens. 1989 Sep;2(9):721-3. doi: 10.1093/ajh/2.9.721.
The constriction produced by a single deep breath was measured simultaneously in two adjacent hand veins in normal subjects. One vein was infused with saline or angiotensin II; the other acted as a control. A dose of angiotensin II (1 pmol/min) that did produce venous constriction directly significantly augmented the constriction caused by deep breath in eight subjects (P less than .01). In a further six subjects the same dose had no effect on venoconstriction caused by infused noradrenaline. We conclude that angiotensin II causes venoconstriction indirectly by augmenting sympathetically mediated responses, possibly by a presynaptic mechanism.
在正常受试者中，同时测量单次深呼吸引起的两条相邻手部静脉的收缩情况。一条静脉注入生理盐水或血管紧张素II；另一条作为对照。1皮摩尔/分钟剂量的血管紧张素II确实直接引起静脉收缩，在8名受试者中显著增强了深呼吸引起的收缩（P小于0.01）。在另外6名受试者中，相同剂量对注入去甲肾上腺素引起的静脉收缩没有影响。我们得出结论，血管紧张素II通过增强交感神经介导的反应间接引起静脉收缩，可能是通过一种突触前机制。
