Endothelium‐dependent relaxation and noradrenaline sensitivity in mesenteric resistance arteries of streptozotocin‐induced diabetic rats
Endothelium‐dependent relaxation and noradrenaline sensitivity in mesenteric resistance arteries of streptozotocin‐induced diabetic rats
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链脲佐菌素诱导的糖尿病大鼠肠系膜阻力动脉的内皮依赖性舒张和去甲肾上腺素敏感性
DOI：
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发表时间：
1992
影响因子：
7.3
通讯作者：
L. Poston
中科院分区：
文献类型：
--
作者：
P. Taylor;Andrew L. McCarthy;C. Thomas;L. Poston
1在对照和链脲佐菌素诱导的糖尿病大鼠的肠系膜阻力动脉中研究去甲肾上腺素敏感性和乙酰胆碱诱导的舒张。2糖尿病大鼠血管对去甲肾上腺素的敏感性明显高于同龄对照组（pEC 50：糖尿病组5.99 ± 0.06，n = 25;对照组5.82 ± 0.03，n = 45，P < 0.05）。3糖尿病组大鼠血管对乙酰胆碱诱导的舒张反应明显低于对照组（pEC 50：糖尿病组6.81 ± 0.17，对照组7.54 ± 0.17，n = 21，P < 0.001）。4在10 μm吲哚美辛存在下，糖尿病大鼠和对照组动脉中乙酰胆碱诱导的舒张作用之间的差异仍然存在（糖尿病大鼠的pEC 50为6.41 ± 0.11，n = 16，对照组为7.59 ± 0.08，n = 20，P < 0.001）。5一氧化氮合酶抑制剂NG-单甲基-m-精氨酸（1-NMMA，1 mm）对糖尿病动脉中乙酰胆碱诱导的舒张产生了深刻的抑制作用，但对对照组产生了部分抑制作用。在对照动脉中，m-NMMA对乙酰胆碱诱导的舒张的不完全抑制是一氧化氮合酶抑制无效的结果，因为替代抑制剂NG-硝基-L-精氨酸甲酯（l-NAME，0.1 mm）导致与l-NMMA在糖尿病动脉中观察到的抑制相似的抑制。因此，与对照动物相比，糖尿病大鼠中通过使用一氧化氮合酶抑制剂测定的乙酰胆碱诱导舒张的内皮源性舒张因子（EDRF）介导成分明显减少。6在进一步的实验中，发现l-NAME增强了对照大鼠对去甲肾上腺素的反应，但在糖尿病动物中没有，这表明糖尿病动物对去甲肾上腺素的异常反应也是由于EDRF释放减少。7对照组和糖尿病大鼠动脉中硝普钠诱导的舒张（非内皮依赖性）相似（糖尿病动脉的pEC 50为7.61 ± 0.13，n = 18，对照组为7.68 ± 0.15，n = 20，P不显著）。8这些结果表明，在链脲佐菌素诱导的糖尿病大鼠的肠系膜阻力动脉中，内皮功能异常，这主要是由于EDRF释放减少。
1 Noradrenaline sensitivity and acetylcholine‐induced relaxation were investigated in mesenteric resistance arteries of control and streptozotocin‐induced diabetic rats. 2 The diabetic rats demonstrated enhanced vascular sensitivity to noradrenaline compared with age‐matched controls (pEC50 5.99 ± 0.06 for diabetic rats, n = 25, versus 5.82 ± 0.03 for controls, n = 45, P < 0.05). 3 Significant impairment of acetylcholine‐induced relaxation was observed in arteries from the diabetic animals compared with controls (pEC50 6.81 ± 0.17 for diabetic rats, n = 21, versus 7.54 ± 0.17 for controls, n = 45, P < 0.001). 4 The difference between acetylcholine‐induced relaxation in diabetic and control arteries remained in the presence of 10 μm indomethacin (pEC50 6.41 ± 0.11 for diabetic rats, n = 16, versus 7.59 ± 0.08 for controls, n = 20, P < 0.001). 5 The nitric oxide synthase inhibitor, NG‐monomethyl‐m‐arginine (l‐NMMA, 1 mm) produced profound inhibition of acetylcholine‐induced relaxation in diabetic arteries but partial inhibition in controls. The incomplete inhibition of acetylcholine‐induced relaxation by m‐NMMA in the control arteries was the result of ineffective inhibition of nitric oxide synthase since an alternative inhibitor, NG‐nitro‐l‐arginine methyl ester (l‐NAME, 0.1 mm), led to similar inhibition to that seen in the diabetic arteries with l‐NMMA. The endothelium‐derived relaxing factor (EDRF)‐mediated component of acetylcholine‐induced relaxation determined by use of the nitric oxide synthase inhibitors was, therefore, apparently reduced in diabetic rats compared with control animals. 6 In further experiments l‐NAME was found to enhance the response to noradrenaline in control rats but not in diabetic animals, suggesting that the abnormal response to noradrenaline in the diabetic animals was also due to reduced EDRF release. 7 Nitroprusside‐induced relaxation (endothelium‐independent) was similar in arteries from control and diabetic rats (pEC50 7.61 ± 0.13 for diabetic arteries, n = 18, versus 7.68 ± 0.15 in the controls, n = 20, P not significant). 8 These results suggest that endothelial function is abnormal in mesenteric resistance arteries of streptozotocin‐induced diabetic rats and that this is predominantly due to reduced EDRF release.
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DOI：
10.1152/ajpheart.1989.257.5.h1327
发表时间：
1989-11
期刊：
The American journal of physiology
影响因子：
--
作者：
B. Tesfamariam;J. Jakubowski;Richard A. Cohen
通讯作者：
B. Tesfamariam;J. Jakubowski;Richard A. Cohen
影响因子：
158.5
作者：
DETEJADA, IS;GOLDSTEIN, I;COHEN, RA
通讯作者：
COHEN, RA
影响因子：
15.9
作者：
TESFAMARIAM, B;BROWN, ML;COHEN, RA
通讯作者：
COHEN, RA
自发释放的内皮衍生舒张因子抑制大鼠主动脉收缩反应。
DOI：
--
发表时间：
1986
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Martin,W;Furchgott,RF;Villani,GM;Jothianandan,D
通讯作者：
Jothianandan,D