Schwieler J H, Nussberger J, Kahan T, Hjemdahl P
Department of Pharmacology, Karolinska Institutet, Stockholm, Sweden.
J Hypertens. 1991 Jun;9(6):487-90. doi: 10.1097/00004872-199106000-00002.
The overflow of endogenous angiotensin-(1-8)octapeptide (angiotensin II) from blood-perfused canine gracilis muscle vasculature in situ was studied. A positive veno-arterial concentration difference for angiotensin II over the gracilis muscle was found, indicating a net generation of angiotensin II under basal conditions. Angiotensin II levels in the venous effluent were elevated during 2 Hz (4-min) nerve stimulation, suggesting enhanced local angiotensin II generation both in the presence and absence of alpha-adrenoceptor blockade. Thus, our results in this in vivo model demonstrate a local overflow of angiotensin II from the skeletal muscle vasculature which can be enhanced by nerve stimulation. Whether this overflow of angiotensin II is due to conversion of circulating angiotensin I to angiotensin II or local de novo synthesis of angiotensin II remains to be established.
研究了原位血液灌注的犬股薄肌血管系统中内源性血管紧张素 -（1 - 8）八肽（血管紧张素II）的溢出情况。发现股薄肌上血管紧张素II存在正的静脉 - 动脉浓度差，表明在基础条件下血管紧张素II有净生成。在2赫兹（4分钟）神经刺激期间，静脉流出液中的血管紧张素II水平升高，这表明在存在和不存在α - 肾上腺素能受体阻断的情况下，局部血管紧张素II生成均增强。因此，我们在这个体内模型中的结果表明，骨骼肌血管系统中血管紧张素II会出现局部溢出，且可通过神经刺激增强。这种血管紧张素II的溢出是由于循环中的血管紧张素I转化为血管紧张素II还是局部从头合成血管紧张素II，仍有待确定。
