Noradrenaline contracts rat retinal arterioles via stimulation of α_<1A>- and (α_<1D>-adrenoceptors
Noradrenaline contracts rat retinal arterioles via stimulation of α_<1A>- and (α_<1D>-adrenoceptors
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去甲肾上腺素通过刺激α_<1A>-和(α_<1D>-肾上腺素受体)收缩大鼠视网膜小动脉
DOI：
10.1016/j.ejphar.2011.10.012
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发表时间：
2011
期刊：
影响因子：
5
通讯作者：
Ishii K
中科院分区：
文献类型：
--
作者：
Mori A;Hanada M;Sakamoto K;Nakahara T;Ishii K
本研究的目的是研究α1肾上腺素受体亚型(S)参与去甲肾上腺素引起的大鼠视网膜小动脉收缩的特征。用配备特殊物镜的数码相机拍摄活体眼底图像。通过测量眼底图像中视网膜小动脉直径的变化，评估视网膜血管反应。连续记录动物的全身血压和心率。用心得安、去甲肾上腺素阻断β1/β2肾上腺素受体后，静脉注射去甲肾上腺素0.03~3μg/kg/min。降低视网膜小动脉直径，升高平均血压，呈剂量依赖关系。最高剂量(3μg/kg/min，iv)去甲肾上腺素使心率略有增加。α1A肾上腺素能受体拮抗剂RS100329(0.1 mg/kg，iv.)和α1D肾上腺素能受体拮抗剂Bmy7378(1 mg/kg，iv.)显著抑制去甲肾上腺素引起的视网膜小动脉收缩和升压反应，而α1B受体拮抗剂L-765314(1 mg/kg，i.v.)没有。α1A肾上腺素能受体激动剂A 61603(0.03~0.3ming/kg/μ)也引起视网膜小动脉收缩反应和升压反应。RS100329(0.1 mg/kg静脉注射)几乎完全阻止上述反应，而BMY 7378(1 mg/kg静脉注射)则不能完全阻止上述反应。这些结果表明，去甲肾上腺素对视网膜小动脉和外周阻力血管的收缩作用至少部分是通过刺激α1A和α1D受体介导的。此外，参与大鼠血管反应的α1肾上腺素能受体亚型(S)在视网膜和外周循环中可能是相似的。
The aim of this study was to characterize the α1-adrenoceptor subtype(s) involved in the noradrenaline-induced contraction of retinal arterioles in rats. In vivo ocular fundus images were captured with a digital camera equipped with a special objective lens. By measuring changes in diameter of retinal arterioles in the fundus images, retinal vascular response was assessed. The systemic blood pressure and heart rate in the animals were also continuously recorded. Following blockade of β1/β2-adrenoceptors with propranolol, noradrenaline (0.03–3μg/kg/min, i.v.) decreased the diameter of retinal arterioles and increased the mean blood pressure in a dose-dependent manner. The highest dose (3μg/kg/min, i.v.) of noradrenaline caused a small increase in heart rate. The α1A-adrenoceptor antagonist RS100329 (0.1mg/kg, i.v.) and the α1D-adrenoceptor antagonist BMY 7378 (1mg/kg, i.v.) significantly prevented noradrenaline-induced contraction of retinal arterioles and pressor responses whereas the α1B-adrenoceptor antagonist L-765314 (1mg/kg, i.v.) did not. The α1A-adrenoceptor agonist, A 61603 (0.03–0.3μg/kg/min, i.v.), also caused contractile responses of retinal arterioles and pressor responses. These responses were almost completely prevented by RS100329 (0.1mg/kg, i.v.), but not by BMY 7378 (1mg/kg, i.v.). These results suggest that the contractile effects of noradrenaline on retinal arterioles and peripheral resistance vessels are, at least in part, mediated by stimulation of α1A- and α1D-adrenoceptors. Furthermore, it is likely that the α1-adrenoceptor subtype(s) involved in rat vascular responses are similar in both retinal and peripheral circulation.