Richardt G, Mayer E, Schömig A
Department of Cardiology, University of Heidelberg, Federal Republic of Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1991 Sep;344(3):297-301. doi: 10.1007/BF00183003.
The effects of exogenous and of endogenous angiotensin on noradrenaline overflow were investigated in saline perfused rat hearts with intact sympathetic nerves. The overflow of endogenous noradrenaline induced by electrical stimulation of the left stellate ganglion was determined in the coronary venous effluent by HPLC. The activity of the renin-angiotensin system was modulated by varying of the nutritional sodium load prior to the experiments. Endogenous angiotensin formation was blocked by angiotensin-converting enzyme inhibitors. Following high sodium intake, both angiotensin II (100 nmol/l) and angiotensin I (1 mumol/l) caused a marked increase of the electrically evoked noradrenaline overflow. After inhibition of the angiotensin-converting enzyme using captopril (350 nmol/l) or ramiprilat (50 nmol/l), angiotensin I (1 mumol/l) did not enhance noradrenaline overflow. This indicates an active cardiac angiotensin conversion, since the sole administration of captopril and ramiprilat did not affect noradrenaline overflow in rats with high sodium intake. Following low sodium intake, neither angiotensin II (100 nmol/l) nor angiotensin I (1 mumol/l) significantly affected noradrenaline overflow. Both captopril and ramiprilat, however, significantly reduced noradrenaline overflow induced by electrical stimulation, suggesting a facilitory action of endogenous angiotensin under these conditions. This concept was substantiated when evaluating the noradrenaline overflow during control stimulations. Following low sodium intake, stimulation evoked noradrenaline overflow was higher as compared to that after nutritional sodium load. The results are in keeping with a sodium-dependent intracardiac formation of angiotensin II which facilitates noradrenaline release from sympathetic nerve terminals. Following low sodium intake, cardiac angiotensin II formation is active, as indicated by the suppression of noradrenaline release by angiotensin-converting enzyme inhibitors and the ineffectiveness of exogenous application of angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)
在交感神经完整的盐灌注大鼠心脏中，研究了外源性和内源性血管紧张素对去甲肾上腺素溢出的影响。通过高效液相色谱法测定冠状静脉流出液中由电刺激左星状神经节诱导的内源性去甲肾上腺素溢出。在实验前，通过改变营养性钠负荷来调节肾素-血管紧张素系统的活性。血管紧张素转换酶抑制剂可阻断内源性血管紧张素的形成。高钠摄入后，血管紧张素 II（100 nmol/l）和血管紧张素 I（1 μmol/l）均导致电诱发的去甲肾上腺素溢出显著增加。使用卡托普利（350 nmol/l）或雷米普利拉（50 nmol/l）抑制血管紧张素转换酶后，血管紧张素 I（1 μmol/l）不再增强去甲肾上腺素溢出。这表明心脏存在活跃的血管紧张素转换，因为单独给予卡托普利和雷米普利拉对高钠摄入大鼠的去甲肾上腺素溢出没有影响。低钠摄入后，血管紧张素 II（100 nmol/l）和血管紧张素 I（1 μmol/l）均未显著影响去甲肾上腺素溢出。然而，卡托普利和雷米普利拉均显著降低了电刺激诱导的去甲肾上腺素溢出，表明在这些条件下内源性血管紧张素具有促进作用。在评估对照刺激期间的去甲肾上腺素溢出时，这一概念得到了证实。低钠摄入后，刺激诱发的去甲肾上腺素溢出高于营养性钠负荷后的溢出。结果与血管紧张素 II 的钠依赖性心脏内形成一致，后者促进去甲肾上腺素从交感神经末梢释放。低钠摄入后，心脏血管紧张素 II 的形成是活跃的，血管紧张素转换酶抑制剂抑制去甲肾上腺素释放以及外源性应用血管紧张素 II 无效均表明了这一点。（摘要截短于250字）
