Webb D J, Seidelin P H, Benjamin N, Collier J G, Struthers A D
Department of Clinical Pharmacology, St George's Hospital Medical School, London, UK.
J Hypertens Suppl. 1988 Dec;6(4):S542-3. doi: 10.1097/00004872-198812040-00170.
In order to determine whether angiotensin II may influence sympathetically mediated arteriolar constriction in man, we have examined the effect of angiotensin II, infused directly into the left brachial artery of normal subjects, on the reduction in forearm blood flow produced by a lower-body negative pressure (LBNP) of 15 mmHg. Angiotensin II (320 fmol/min) caused no reduction in blood flow when given alone but significantly augmented the reduction in blood flow in response to LBNP. The same dose of angiotensin II did not affect a similar reduction in forearm blood flow produced by infused noradrenaline (12.5-50 ng/min). We conclude that angiotensin II augments sympathetically mediated constriction of resistance vessels in man at concentrations with no direct effect on vessel tone. The lack of an effect of angiotensin II on constriction in response to infused noradrenaline suggests the involvement of a presynaptic mechanism.
为了确定血管紧张素II是否会影响人体交感神经介导的小动脉收缩，我们研究了直接注入正常受试者左肱动脉的血管紧张素II对15 mmHg下体负压（LBNP）引起的前臂血流减少的影响。血管紧张素II（320 fmol/分钟）单独给药时不会导致血流减少，但会显著增强对LBNP的血流减少反应。相同剂量的血管紧张素II对注入去甲肾上腺素（12.5 - 50 ng/分钟）引起的前臂血流类似减少没有影响。我们得出结论，血管紧张素II在对血管张力无直接影响的浓度下增强人体交感神经介导的阻力血管收缩。血管紧张素II对注入去甲肾上腺素引起的收缩无影响表明涉及一种突触前机制。
