Kahan T, Lindqvist M, Nussberger J, Melcher A, Hjemdahi P
Division of Internal Medicine, Karolinska institutet, Danderyd Hospital, Sweden.
Acta Physiol Scand. 1997 Feb;159(2):107-11. doi: 10.1046/j.1365-201X.1997.580330000.x.
Complex interactions appear to exist between the renin-angiotensin system and sympathetic neurotransmission, and sympathetic activity may influence local angiotensin II formation. Arterial and forearm venous plasma levels of angiotensin I and II were therefore studied in 11 healthy males at rest during sympathetic activation elicited by mental stress, and during adrenaline induced vasodilation. Specific assays for angiotensin-(1-8) octapeptide and for angiotensin-(1-10) decapeptide (i.e. angiotensin II and I, respectively), were used. Special precautions to minimize ex vivo formation and/or degradation of angiotensins were employed. Mental stress increased regional noradrenaline overflow three-fold, with a concomitant three-fold increase in forearm blood flow, whereas intravenous adrenaline infusion increased forearm blood flow two-fold and noradrenaline overflow four-old. There was a constant positive veno-arterial concentration difference for angiotensin I under all conditions tested, compatible with local angiotensin I formation. We found no veno-arterial concentration difference for angiotensin II or regional net angiotensin II overflow under the conditions tested. These results in the forearm circulation support previous animal experimental evidence in skeletal muscle and provide no evidence in favour of a de novo formation of angiotensin II in skeletal muscle in vivo during basal conditions. Furthermore, sympathetic nerve stimulation does not seem to enhance angiotensin II generation importantly in this vascular bed.
肾素-血管紧张素系统与交感神经传递之间似乎存在复杂的相互作用，交感神经活动可能会影响局部血管紧张素II的形成。因此，我们对11名健康男性在静息状态下、精神应激引起交感神经激活期间以及肾上腺素诱导血管舒张期间，研究了动脉和前臂静脉血浆中血管紧张素I和II的水平。采用了针对血管紧张素-(1-8)八肽和血管紧张素-(1-10)十肽（即分别为血管紧张素II和I）的特异性检测方法。采取了特殊预防措施以尽量减少血管紧张素在体外的形成和/或降解。精神应激使局部去甲肾上腺素溢出增加了三倍，同时前臂血流量增加了三倍，而静脉注射肾上腺素使前臂血流量增加了两倍，去甲肾上腺素溢出增加了四倍。在所有测试条件下，血管紧张素I的静脉-动脉浓度差始终为正值，这与局部血管紧张素I的形成相符。在测试条件下，我们未发现血管紧张素II的静脉-动脉浓度差或局部血管紧张素II净溢出。前臂循环的这些结果支持了先前在骨骼肌中的动物实验证据，且未提供在基础条件下体内骨骼肌中从头合成血管紧张素II的证据。此外，交感神经刺激似乎并未在该血管床中显著增强血管紧张素II的生成。
