血管紧张素对猫股动脉血管张力和肾上腺素能神经传递的调节作用。

Angiotensin modulation of vascular tone and adrenergic neurotransmission in cat femoral arteries.

Encabo A, Ferrer M, Marín J, Balfagón G

Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, Spain.

Gen Pharmacol. 1994 Dec;25(8):1691-7. doi: 10.1016/0306-3623(94)90373-5.

Abstract

AI and AII induced contractions in cat femoral arteries, which were inhibited by saralasin. 2. The response to AI was reduced by captopril and endothelium removal and by chymostatin in endothelium-denuded segments. 3. AII contractions were increased by indomethacin, L-NAME and endothelium removal. 4. AII and AI facilitated the adrenergic neurotransmission. This facilitation was inhibited by saralasin and/or captopril. 5. These data suggest: (1) AI is converted into AII in the endothelial and adventitial layer; (2) the contractions caused by AI and AII are mediated by AII receptors and are modulated by endothelial release of NO and PGI2; and (3) the existence of presynaptic AII receptors mediating the facilitation of neurotransmission caused by AI and AII.

摘要

血管紧张素Ⅰ（AI）和血管紧张素Ⅱ（AII）可引起猫股动脉收缩，而沙拉新可抑制这种收缩。2. 在去内皮的血管段中，卡托普利、去除内皮以及抑肽酶均可降低对AI的反应。3. 吲哚美辛、L- NAME和去除内皮可增强AII引起的收缩。4. AII和AI可促进肾上腺素能神经传递。这种促进作用可被沙拉新和/或卡托普利抑制。5. 这些数据表明：（1）AI在内皮和外膜层转化为AII；（2）AI和AII引起的收缩由AII受体介导，并受内皮释放的一氧化氮（NO）和前列环素（PGI2）调节；（3）存在突触前AII受体，介导AI和AII引起的神经传递促进作用。