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.
作者信息
Encabo A, Ferrer M, Marín J, Balfagón G
机构信息
Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid, Spain.
出版信息
Gen Pharmacol. 1994 Dec;25(8):1691-7. doi: 10.1016/0306-3623(94)90373-5.
PMID:7721047
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。
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