Effects of chronic in vivo administration of nitroglycerine on ACh-induced endothelium-dependent relaxation in rabbit cerebral arteries

被引:7
|
作者
Watanabe, Y. [1 ]
Kusama, N. [1 ,2 ]
Itoh, T. [1 ]
机构
[1] Nagoya City Univ, Grad Sch Med Sci, Dept Pharmacol, Nagoya, Aichi 4678601, Japan
[2] Nagoya City Univ, Grad Sch Med Sci, Dept Anesthesiol & Med Crisis Management, Nagoya, Aichi, Japan
关键词
middle cerebral artery; posterior cerebral artery; endothelium-dependent relaxation; nitric oxide; endothelium-derived hyperpolarizing factor; nitroglycerine; nitrate tolerance; rabbit;
D O I
10.1038/sj.bjp.0707562
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Background and purpose: In the setting of nitrate tolerance, endothelium-dependent relaxation is reduced in several types of peripheral vessels. However, it is unknown whether chronic in vivo administration of nitroglycerine modulates such relaxation in cerebral arteries. Experimental approach: Isometric force and smooth muscle cell membrane potential were measured in endothelium-intact strips from rabbit middle cerebral artery (MCA) and posterior cerebral artery (PCA). Key results: ACh (0.1-10 mu M) concentration-dependently induced endothelium-dependent relaxation during the contraction induced by histamine in both MCA and PCA. Chronic ( 10 days) in vivo administration of nitroglycerine reduced the ACh-induced relaxation in PCA but not in MCA, in the presence of the cyclooxygenase inhibitor diclofenac ( 3 mu M). In the presence of the NO-synthase inhibitor N-omega-nitro-L-arginine(L-NNA, 0.1 mM) plus diclofenac, in MCA from both nitroglycerine-untreated control and-treated rabbits, ACh (0.1-10 mu M) induced a smooth muscle cell hyperpolarization and relaxation, and these were blocked by the small-conductance Ca2+-activated K+-channel inhibitor apamin ( 0.1 mu M), but not by the large- and intermediate-conductance Ca2+-activated K+-channel inhibitor charybdotoxin ( 0.1 mu M). In contrast, in PCA, ACh (< 3 mu M) induced neither hyperpolarization nor relaxation under these conditions, suggesting that the endothelium-derived relaxing factor is NO in PCA, whereas endothelium-derived hyperpolarizing factor ( EDHF) plays a significant role in MCA. Conclusions and implications: It is suggested that in rabbit cerebral arteries, the function of the endothelium-derived relaxing factor NO and that of EDHF may be modulated differently by chronic in vivo administration of nitroglycerine.
引用
收藏
页码:132 / 139
页数:8
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