Effect of L-arginine on reactivity of hamster cheek pouch arterioles during diabetes mellitus.

W G Mayhan, K P Patel, G M Sharpe
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引用次数: 14

Abstract

The goal of this study was to determine whether exogenous application of L-arginine could restore impaired agonist-induced increases in arteriolar diameter during diabetes mellitus. We used intravital microscopy to examine reactivity of cheek pouch arterioles (50 microns in diameter) in nondiabetic and diabetic (2 weeks after injection of streptozotocin) hamsters in response to histamine and substance P. In nondiabetic hamsters histamine (1.0 and 5.0 microM) dilated cheek pouch arterioles by 15 +/- 1 and 22 +/- 1%, respectively, and substance P (50 and 100 nM) dilated arterioles by 14 +/- 3 and 21 +/- 4%, respectively. In addition, dilatation of arterioles in response to histamine and substance P in nondiabetic hamsters was abolished by application of an enzymatic inhibitor of nitric oxide synthase (L-NMMA). In contrast, histamine- and substance P-induced increases in arteriolar diameter were markedly reduced in diabetic hamsters. Histamine (1.0 and 5.0 microM) dilated arterioles by only 5 +/- 1 and 4 +/- 2%, respectively, and substance P (50 and 100 nM) dilated arterioles by only 6 +/- 2 and 5 +/- 3%, respectively (p < 0.05 vs. nondiabetic hamsters). Nitroglycerin produced similar vasodilatation in nondiabetic and diabetic hamsters. Next, we examined whether exogenous application of L-arginine (100 microM) could restore impaired histamine- and substance P-induced increases in arteriolar diameter in diabetic hamsters. We found that L-arginine did not restore altered nitric oxide synthase-dependent vasodilatation in diabetic hamsters. These findings suggest that short-term diabetes mellitus alters agonist-induced increases in arteriolar diameter. In addition, the mechanism of altered arteriolar reactivity during diabetes mellitus does not appear to be related to an impaired availability of L-arginine.

l -精氨酸对糖尿病仓鼠颊袋小动脉反应性的影响。
本研究的目的是确定外源性应用l -精氨酸是否可以恢复激动剂引起的糖尿病患者动脉直径的增加。我们用活体显微镜观察了非糖尿病和糖尿病(注射链脲佐菌素2周后)仓鼠颊袋小动脉(直径50微米)对组胺和P物质的反应性。在非糖尿病仓鼠中,组胺(1.0和5.0微米)分别使颊袋小动脉扩张了15 +/- 1%和22 +/- 1%,P物质(50和100 nM)分别使颊袋小动脉扩张了14 +/- 3%和21 +/- 4%。此外,应用一氧化氮合酶酶抑制剂(L-NMMA)可消除非糖尿病仓鼠对组胺和P物质反应的小动脉扩张。相比之下,组胺和p物质引起的糖尿病仓鼠小动脉直径的增加明显减少。组胺(1.0和5.0 μ m)分别使小动脉扩张5 +/- 1和4 +/- 2%,P物质(50和100 μ m)分别使小动脉扩张6 +/- 2和5 +/- 3%(与非糖尿病仓鼠相比P < 0.05)。硝酸甘油在非糖尿病和糖尿病仓鼠中产生类似的血管扩张。接下来,我们研究了外源性应用l -精氨酸(100 μ m)是否可以恢复组胺和p物质引起的糖尿病仓鼠动脉直径的损伤。我们发现l -精氨酸不能恢复糖尿病仓鼠一氧化氮合酶依赖性血管舒张。这些发现表明,短期糖尿病改变激动剂诱导的小动脉直径增加。此外,糖尿病期间动脉反应性改变的机制似乎与l -精氨酸可用性受损无关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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