首页> 外文期刊>European Journal of Pharmacology: An International Journal >Noradrenaline contracts rat retinal arterioles via stimulation of α 1A- and α 1D-adrenoceptors
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Noradrenaline contracts rat retinal arterioles via stimulation of α 1A- and α 1D-adrenoceptors

机译:去甲肾上腺素通过刺激α1A-和α1D-肾上腺素受体收缩大鼠视网膜小动脉

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摘要

The aim of this study was to characterize the α 1- 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 β 1/ β 2-adrenoceptors with propranolol, noradrenaline (0.03-3 μg/kg/min, i.v.) decreased the diameter of retinal arterioles and increased the mean blood pressure in a dose-dependent manner. The highest dose (3 μg/kg/min, i.v.) of noradrenaline caused a small increase in heart rate. The α 1A-adrenoceptor antagonist RS100329 (0.1 mg/kg, i.v.) and the α 1D-adrenoceptor antagonist BMY 7378 (1 mg/kg, i.v.) significantly prevented noradrenaline-induced contraction of retinal arterioles and pressor responses whereas the α 1B-adrenoceptor antagonist L-765314 (1 mg/kg, i.v.) did not. The α 1A-adrenoceptor agonist, A 61603 (0.03-0.3 μg/kg/min, i.v.), also caused contractile responses of retinal arterioles and pressor responses. These responses were almost completely prevented by RS100329 (0.1 mg/kg, i.v.), but not by BMY 7378 (1 mg/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 α 1A- and α 1D-adrenoceptors. Furthermore, it is likely that the α 1-adrenoceptor subtype(s) involved in rat vascular responses are similar in both retinal and peripheral circulation.
机译:这项研究的目的是表征参与去甲肾上腺素诱导的大鼠视网膜小动脉收缩的α1-肾上腺素受体亚型。用配备有特殊物镜的数码相机捕获体内眼底图像。通过测量眼底图像中视网膜小动脉直径的变化,可以评估视网膜血管反应。还连续记录动物的全身血压和心率。用普萘洛尔阻断β1 /β2肾上腺素能受体后,去甲肾上腺素(0.03-3μg/ kg / min,静脉内)降低了视网膜小动脉的直径,并以剂量​​依赖性方式增加了平均血压。去甲肾上腺素的最高剂量(3μg/ kg / min,i.v.)引起心率小幅增加。 α1A肾上腺素受体拮抗剂RS100329(0.1 mg / kg,iv)和α1D肾上腺素受体拮抗剂BMY 7378(1 mg / kg,iv)显着阻止去甲肾上腺素诱导的视网膜小动脉收缩和升压反应,而α1B-肾上腺素受体拮抗剂L-765314(1 mg / kg,静脉注射)则没有。 α1A肾上腺素受体激动剂A 61603(0.03-0.3μg/ kg / min,静脉内)也引起视网膜小动脉的收缩反应和升压反应。 RS100329(0.1 mg / kg,i.v.)几乎完全阻止了这些反应,但BMY 7378(1 mg / kg,i.v.)并未完全阻止。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地由α1A-和α1D-肾上腺素受体的刺激介导。此外,在视网膜和外周循环中,参与大鼠血管反应的α1-肾上腺素受体亚型可能相似。

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