Endothelin-induced changes in blood flow in STZ-diabetic and non-diabetic rats: relation to nitric oxide synthase and cyclooxygenase inhibition.
Endothelin-induced changes in blood flow in STZ-diabetic and non-diabetic rats: relation to nitric oxide synthase and cyclooxygenase inhibition.
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DOI：
10.1007/s12576-011-0171-x
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发表时间：
2011-11
影响因子：
2.3
通讯作者：
Granstam, Elisabet
中科院分区：
文献类型：
--
作者：
Granstam, Sven-Olof;Granstam, Elisabet
本研究采用微球法，观察了内皮素-1（ET-1）对健康和链脲佐菌素（STZ）糖尿病大鼠血流动力学的影响，以及用L-硝基精氨酸甲酯（L-NAME）和环氧化酶抑制剂吲哚美辛抑制一氧化氮（NO）合酶对ET-1的影响。在糖尿病血管并发症的相关组织（如肾脏、眼睛、大脑、心脏和骨骼肌）中测量血流量（Q），主要关注眼循环。在静息条件下，糖尿病动物中发现肾血管收缩的证据。在这两组中，L-NAME的管理减少Q在所有调查的组织表明基础NO的影响。在正常大鼠中，ET-1引起血压显著升高，除眼脉络膜和脑中引起Q增加外，所有组织中均出现强烈的血管收缩。在STZ糖尿病大鼠中，ET-1的作用不太明显。用L-NAME预处理，而不是环氧合酶抑制剂，取消了ET-1诱导的脉络膜血管舒张。给药ETA受体拮抗剂BQ-123仅在糖尿病动物中减少ET-1诱导的脉络膜血管舒张。总之，STZ-糖尿病动物中血管内皮对ET-1反应改变的证据尤其在眼循环中发现。研究结果表明，在正常和STZ-糖尿病动物的受体的差异参与ET-1的反应。
In this study, using the microsphere method, the hemodynamic response to endothelin-1 (ET-1) in healthy and streptozotocin (STZ)-diabetic rats was evaluated as well as the influences of inhibition of nitric oxide (NO)-synthase using L-NAME (Nω-nitro-l-arginine methyl ester) and the cyclooxygenase inhibitor indomethacin. Blood flow (Q) was measured in tissues of interest for vascular complications in diabetes such as kidney, eye, brain, heart and skeletal muscle with the main focus on ophthalmic circulation. Under resting conditions, evidence for renal vasoconstriction was found in diabetic animals. In both groups, administration of L-NAME reduced Q in all investigated tissues indicating a basal NO influence. In the normal rats, ET-1 induced a significant increase in blood pressure and intense vasoconstriction in all tissues except in the choroid of the eye and in the brain, where it induced an increased Q. In the STZ-diabetic rats, effects of ET-1 were less pronounced. Pretreatment with L-NAME, but not the cyclooxygenase inhibitor, abolished the ET-1-induced vasodilation in the choroid of both groups. Administration of ET A receptor antagonist BQ-123 reduced the ET-1-induced vasodilation in the choroid only in diabetic animals. In conclusion, evidence for altered vascular endothelial response to ET-1 in STZ-diabetic animals was found particularly in the ophthalmic circulation. The findings suggest differential involvement of receptors in the response to ET-1 in normal and STZ-diabetic animals.
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