Department of Molecular Pharmacology, Kitasato University School of Pharmaceutical Sciences, 5-9-1 Shirokane, Minato-ku, Tokyo, 108-8641, Japan.
Naunyn Schmiedebergs Arch Pharmacol. 2010 Aug;382(2):119-26. doi: 10.1007/s00210-010-0526-5. Epub 2010 May 26.
The aim of this study was to examine whether stimulation of beta(3)-adrenoceptors dilates rat retinal blood vessels and how diabetes affects the vasodilator responses. Images of ocular fundus were captured with an original high-resolution digital fundus camera in vivo. The retinal vascular responses were evaluated by measuring diameter of retinal blood vessels contained in the digital images. Both systemic blood pressure and heart rate (HR) were continuously recorded. The beta(3)-adrenoceptor agonist CL316243 (0.3-10 microg/kg/min, i.v.) increased diameter of retinal arterioles (at 10 microg/kg/min, a 31% increase) and decreased mean blood pressure (at 10 microg/kg/min, a 21% decrease) in a dose-dependent manner. CL316243 produced a small but significant increase in HR (at 10 microg/kg/min, a 9% increase). Both SR59230A (1 mg/kg, i.v.) and L-748337 (50 microg/kg, i.v.), beta(3)-adrenoceptor antagonists, significantly prevented CL316243-induced retinal vasodilator responses. Similar observations were made with another beta(3)-adrenoceptor agonist, BRL37344. The beta(2)-adrenoceptor agonist salbutamol also increased diameter of retinal arterioles (at 10 microg/kg/min, a 43% increase), whereas the drug produced greater decrease in blood pressure (at 10 microg/kg/min, a 46% decrease) and increase in HR (at 10 microg/kg/min, a 16% increase), compared with beta(3)-adrenoceptor agonists. The retinal vasodilator responses to CL316243 and BRL37344 observed under blockade of beta(1)/beta(2)-adrenoceptors with propranolol (2 mg/kg, i.v. bolus followed by 100 microg/kg/min infusion) were unaffected 2 weeks after induction of diabetes by the combination of streptozotocin treatment and D: -glucose feeding. On the other hand, the vasodilator responses to salbutamol of retinal arterioles were significantly reduced in diabetic rats. These results suggest that stimulation of beta(3)-adrenoceptors causes the vasodilation of retinal arterioles in vivo and the vasodilator responses are unaffected at the early stage of diabetes.
本研究旨在探讨β3-肾上腺素受体的刺激是否会扩张大鼠视网膜血管,以及糖尿病如何影响血管舒张反应。通过体内原创高分辨率数字眼底相机捕获眼部眼底图像。通过测量数字图像中包含的视网膜血管直径来评估视网膜血管反应。连续记录全身血压和心率(HR)。β3-肾上腺素受体激动剂 CL316243(0.3-10μg/kg/min,静脉内)以剂量依赖性方式增加视网膜小动脉直径(在 10μg/kg/min 时增加 31%)并降低平均血压(在 10μg/kg/min 时降低 21%)。CL316243 使 HR 略有但显著增加(在 10μg/kg/min 时增加 9%)。β3-肾上腺素受体拮抗剂 SR59230A(1mg/kg,静脉内)和 L-748337(50μg/kg,静脉内)均显著阻止 CL316243 引起的视网膜血管舒张反应。用另一种β3-肾上腺素受体激动剂 BRL37344 也观察到类似的观察结果。β2-肾上腺素受体激动剂沙丁胺醇也增加视网膜小动脉直径(在 10μg/kg/min 时增加 43%),而与β3-肾上腺素受体激动剂相比,该药物使血压降低更大(在 10μg/kg/min 时降低 46%)和 HR 增加(在 10μg/kg/min 时增加 16%)。在用普萘洛尔(2mg/kg,静脉内推注,然后以 100μg/kg/min 输注)阻断β1/β2-肾上腺素受体后观察到 CL316243 和 BRL37344 的视网膜血管舒张反应不受链脲佐菌素治疗和 D:-葡萄糖喂养联合诱导糖尿病 2 周后的影响。另一方面,糖尿病大鼠视网膜小动脉对沙丁胺醇的血管舒张反应明显降低。这些结果表明,刺激β3-肾上腺素受体可引起体内视网膜小动脉扩张,糖尿病早期血管舒张反应不受影响。