Gender Differences in Vascular Reactivity of Aortas from Streptozotocin-Induced Diabetic Mice
Gender Differences in Vascular Reactivity of Aortas from Streptozotocin-Induced Diabetic Mice
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DOI：
10.1248/bpb.33.1692
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发表时间：
2010-10-01
影响因子：
2
通讯作者：
Kamata, Katsuo
中科院分区：
文献类型：
--
作者：
Takenouchi, Yasuhiro;Kobayashi, Tsuneo;Kamata, Katsuo
本研究的目的是评估糖尿病相关的血管反应性的性别差异，在小鼠动脉瘤。糖尿病是缺血性心脏病、脑缺血和动脉粥样硬化的危险因素，在这些疾病中内皮功能障碍起致病作用。我们研究了从链脲佐菌素（STZ）诱导的1型糖尿病小鼠和年龄匹配的对照小鼠中分离的血管反应，并寻找糖尿病诱导的这些反应变化的性别差异。对于每个性别，糖尿病小鼠的血浆脂联素水平低于对照组，雌性显著高于雄性。乙酰胆碱（ACh）诱导的内皮依赖性舒张主动脉环受损（与年龄匹配的对照组相比）在糖尿病雄性小鼠，但不糖尿病雌性小鼠。硝普钠诱导的内皮非依赖性主动脉舒张在雄性或雌性小鼠中均未被糖尿病改变。去甲肾上腺素诱导的主动脉收缩在糖尿病雌性小鼠中增强（与对照组相比），但在糖尿病雄性小鼠中没有增强，而在N-G-硝基-L-精氨酸存在下，两种性别都没有表现出显著的糖尿病诱导的这种收缩变化。可乐定诱导和胰岛素诱导的内皮依赖性主动脉舒张功能仅在糖尿病女性组中受损（与年龄匹配的对照组相比）。这些结果表明：a）在雄性糖尿病小鼠中，表现出低脂联素水平，这是由ACh诱导的主动脉舒张和一氧化氮（NO）产生的损害，而B）在雌性糖尿病小鼠中，存在由胰岛素和可乐定诱导的主动脉舒张的损害。
The aim of the present study was to assess gender differences in diabetes-related vascular reactivity in murine aortas. Diabetes is a risk factor for ischemic heart disease, cerebral ischemia, and atherosclerosis, conditions in which endothelial dysfunction plays a pathogenetic role. We examined vascular responses in aortas isolated from streptozotocin (STZ)-induced type 1 diabetic mice and age-matched control mice, and looked for gender differences in the diabetes-induced changes in these responses. For each gender, the plasma adiponectin levels were lower in diabetic mice than in the controls, and they were significantly higher in females than in males. The acetylcholine (ACh)-induced endothelium-dependent relaxation of aortic rings was impaired (vs. that in the age-matched controls) in diabetic male mice, but not in diabetic female mice. The sodium nitroprusside-induced endothelium-independent aortic relaxation was not altered by diabetes in either male or female mice. The norepinephrine-induced aortic contraction was enhanced (vs. that in the control group) in diabetic female mice, but not in diabetic male mice, whereas in the presence of N-G-nitro-L-arginine neither gender exhibited a significant diabetes-induced change in this contraction. The clonidine-induced and insulin-induced endothelium-dependent aortic relaxations were impaired only in the diabetic female group (vs. the age-matched controls). These results suggest that: a) in male diabetic mice, which exhibited low adiponectin levels, these were impairments of both the aortic relaxation and nitric oxide (NO) production induced by ACh, whereas b) in female diabetic mice, there were impairments of the aortic relaxations induced by both insulin and clonidine.