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Cytokines and cytokine profiles in human autoimmune diseases and animal models of autoimmunity.细胞因子和细胞因子谱在人类自身免疫性疾病和自身免疫动物模型中的作用。
Mediators Inflamm. 2009;2009:979258. doi: 10.1155/2009/979258. Epub 2009 Oct 26.
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Endothelial dysfunction in diabetes: from mechanisms to therapeutic targets.糖尿病中的内皮功能障碍：从机制到治疗靶点
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Losartan improves impaired nitric oxide synthase-dependent dilatation of cerebral arterioles in type 1 diabetic rats.氯沙坦可改善1型糖尿病大鼠脑动脉中一氧化氮合酶依赖性舒张功能受损的情况。
Brain Res. 2008 May 13;1209:128-35. doi: 10.1016/j.brainres.2008.03.020. Epub 2008 Mar 21.
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Acute infusion of nicotine impairs nNOS-dependent reactivity of cerebral arterioles via an increase in oxidative stress.急性输注尼古丁会通过增加氧化应激来损害脑动脉小血管中依赖于神经元型一氧化氮合酶的反应性。
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Inhibition of NAD(P)H oxidase alleviates impaired NOS-dependent responses of pial arterioles in type 1 diabetes mellitus.抑制NAD(P)H氧化酶可减轻1型糖尿病软脑膜小动脉中一氧化氮合酶依赖性反应受损的情况。
Microcirculation. 2006 Oct-Nov;13(7):567-75. doi: 10.1080/10739680600885194.
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Diabetes-induced cerebrovascular dysfunction: role of poly(ADP-ribose) polymerase.糖尿病诱导的脑血管功能障碍：聚（ADP - 核糖）聚合酶的作用
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Interactions between endothelin and nitric oxide in the regulation of vascular tone in obesity and diabetes.肥胖与糖尿病中内皮素和一氧化氮在血管张力调节中的相互作用。
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内皮素-1 受体抑制可改善 1 型糖尿病大鼠脑小动脉中一氧化氮合酶依赖性舒张功能障碍。

Inhibition of endothelin-1 receptors improves impaired nitric oxide synthase-dependent dilation of cerebral arterioles in type-1 diabetic rats.

机构信息

Department of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska 68198-5850, USA.

出版信息

Microcirculation. 2010 Aug;17(6):439-46. doi: 10.1111/j.1549-8719.2010.00042.x.

DOI:10.1111/j.1549-8719.2010.00042.x
PMID:20690982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2922043/
Abstract

OBJECTIVE

Endothelin-1 has been implicated in the pathogenesis of many cardiovascular-related diseases, including diabetes. The goal of this study was to examine the influence of endothelin-1 receptors (ET(A)) in impaired responses of cerebral (pial) arterioles in type-1 diabetic rats.

METHODS

We measured responses of cerebral arterioles in non-diabetic rats to endothelial nitric oxide synthase (eNOS)-dependent (ADP), neuronal nitric oxide synthase (nNOS)-dependent (N-methyl-d-aspartic acid [NMDA]) and NOS-independent (nitroglycerin) agonists before and during application of BQ-123, an ET(A) receptor antagonist. In addition, we harvested brain tissue from non-diabetic and diabetic rats to measure the production of superoxide anion under basal conditions and during inhibition of ET(A) receptors.

RESULTS

We found that diabetes specifically impaired eNOS- and nNOS-dependent reactivity of cerebral arterioles, but did not alter NOS-independent vasodilation. In addition, while BQ-123 did not alter responses in non-diabetic rats, BQ-123 restored impaired eNOS- and nNOS-dependent vasodilation in diabetic rats. Further, superoxide production was higher in brain tissue from diabetic rats compared with non-diabetic rats under basal conditions and BQ-123 decreased basal production of superoxide in diabetic rats.

CONCLUSION

We suggest that activation of ET(A) receptors during type-1 diabetes mellitus plays an important role in impaired eNOS- and nNOS-dependent dilation of cerebral arterioles.

摘要

目的

内皮素-1 与许多心血管相关疾病的发病机制有关，包括糖尿病。本研究旨在探讨 1 型糖尿病大鼠脑（脑膜）小动脉内皮一氧化氮合酶（eNOS）依赖性（ADP）、神经元一氧化氮合酶（nNOS）依赖性（N-甲基-D-天冬氨酸 [NMDA]）和非一氧化氮合酶依赖性（硝酸甘油）激动剂作用受损时内皮素-1 受体（ET(A)）的影响。

方法

我们在应用 ET(A)受体拮抗剂 BQ-123 前后，测量了非糖尿病大鼠脑小动脉对内皮型一氧化氮合酶（eNOS）依赖性（ADP）、神经元型一氧化氮合酶（nNOS）依赖性（N-甲基-D-天冬氨酸 [NMDA]）和非一氧化氮合酶依赖性（硝酸甘油）激动剂的反应，并测量了基础条件下和抑制 ET(A)受体时大脑组织中超氧阴离子的产生。此外，我们还从非糖尿病和糖尿病大鼠中采集脑组织，以测量基础条件下和抑制 ET(A)受体时超氧阴离子的产生。

结果

我们发现糖尿病特异性地损害了脑小动脉的 eNOS 和 nNOS 依赖性反应，但没有改变非一氧化氮合酶依赖性血管舒张。此外，虽然 BQ-123 没有改变非糖尿病大鼠的反应，但 BQ-123 恢复了糖尿病大鼠中受损的 eNOS 和 nNOS 依赖性血管舒张。此外，在基础条件下，糖尿病大鼠脑组织中超氧阴离子的产生高于非糖尿病大鼠，BQ-123 降低了糖尿病大鼠基础条件下超氧阴离子的产生。

结论

我们认为，1 型糖尿病期间 ET(A)受体的激活在 eNOS 和 nNOS 依赖性脑小动脉舒张受损中起重要作用。