Dominiak P, Elfrath A, Türck D
Clin Exp Hypertens A. 1987;9(2-3):369-73. doi: 10.3109/10641968709164199.
Acute administration of captopril has been reported to decrease noradrenaline (NA) release from the sympathetic nerves. In this study the chronic effects of ramipril on the sympathetic nervous system of male spontaneously hypertensive rats (SHR) have been investigated and compared to those of captopril and enalapril. As parameters for catecholamine biosynthesis and storage, the activity of tyrosine hydroxylase and the catecholamine content of the hearts and the adrenal medulla were measured by HPLC in treated and control SHR. To assess sympathetic outflow plasma NA and adrenaline (A) levels were determined during preganglionic stimulation (PS) of the spinal cord. Under none of these drugs could differences be observed between the treated and control animals, neither in the biosynthesis and storage of catecholamines in the heart and adrenal medulla nor in the sympathetic outflow. However, the dose response curves of blood pressure vs PS were significantly shifted to the right when ACE-inhibitors were administered, most strongly by ramipril. In view of the unaltered presynaptic sympathetic function long term treatment with ACE-inhibitors is suggested to increase bradykinin and angiotensin I. Bradykinin and angiotensin I are capable of releasing NA and A from the adrenal medulla, like angiotensin II.
据报道，卡托普利急性给药可减少交感神经去甲肾上腺素（NA）的释放。在本研究中，已对雷米普利对雄性自发性高血压大鼠（SHR）交感神经系统的慢性影响进行了研究，并与卡托普利和依那普利的影响进行了比较。作为儿茶酚胺生物合成和储存的参数，通过高效液相色谱法（HPLC）测定了治疗组和对照组SHR心脏和肾上腺髓质中酪氨酸羟化酶的活性以及儿茶酚胺含量。为了评估交感神经输出，在脊髓节前刺激（PS）期间测定血浆NA和肾上腺素（A）水平。在这些药物处理下，无论是在心脏和肾上腺髓质中儿茶酚胺的生物合成和储存方面，还是在交感神经输出方面，治疗组和对照组动物之间均未观察到差异。然而，当给予血管紧张素转换酶抑制剂（ACE抑制剂）时，血压与PS的剂量反应曲线明显右移，雷米普利的影响最为显著。鉴于突触前交感神经功能未改变，提示长期使用ACE抑制剂可增加缓激肽和血管紧张素I。缓激肽和血管紧张素I能够像血管紧张素II一样从肾上腺髓质释放NA和A。
