Augmented Endothelium-Derived Hyperpolarizing Factor-Mediated Relaxations Attenuate Endothelial Dysfunction in Femoral and Mesenteric, but Not in Carotid Arteries from Type I Diabetic Rats
Augmented Endothelium-Derived Hyperpolarizing Factor-Mediated Relaxations Attenuate Endothelial Dysfunction in Femoral and Mesenteric, but Not in Carotid Arteries from Type I Diabetic Rats
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增强内皮衍生的超极化因子介导的松弛可减轻 I 型糖尿病大鼠股动脉和肠系膜的内皮功能障碍，但不能减轻颈动脉的内皮功能障碍
DOI：
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发表时间：
2006
影响因子：
3.5
通讯作者：
P. Vanhoutte
中科院分区：
文献类型：
--
作者：
Yi;D. Ku;R. Man;P. Vanhoutte
个别血管床表现出血管反应性的差异。本研究探讨链脲佐菌素诱导的1型糖尿病对大鼠颈动脉、股动脉和肠系膜动脉内皮依赖性反应的影响。带内皮和不带内皮的环悬浮在器官室中进行等距张力记录，用苯肾上腺素收缩并暴露于浓度增加的乙酰胆碱中。在颈动脉和股动脉中，乙酰胆碱产生浓度依赖性和内皮依赖性松弛，这种松弛被n ω-硝基-l-精氨酸甲酯（l-NAME；特异性一氧化氮合酶抑制剂）所消除，并且在链脲佐菌素处理大鼠（stz -大鼠）的制剂中轻微受损。这种损伤可由l-精氨酸预防。在用l-NAME培养的股动脉中，乙酰胆碱引起内皮依赖性收缩，这种收缩被3-[（6-氨基-（4-氯苯磺酰基）-2-甲基-5,6,7,8-四水合酶]-1-酰基）丙酸（S18886）（血栓素A2/前列腺素h2受体拮抗剂）消除，并被吲哚美辛（环氧化酶抑制剂）逆转为松弛。后一种松弛被白蜡毒素和维生素抑制，提示内皮依赖性超极化因子（EDHF）的作用。这种edhf介导的成分在stz大鼠的动脉中略有增加。在肠系膜动脉中，l-NAME仅部分抑制对乙酰胆碱的松弛，而l-NAME抗性成分则被肉毒杆菌毒素加维生素所消除。在stz大鼠肠系膜动脉中，l- name对乙酰胆碱的敏感松弛减少，edhf成分增加。这些发现证明了大鼠动脉内皮依赖性反应的显著异质性及其在I型糖尿病过程中的差异适应。特别是，edhf介导的成分不仅补偿了股动脉和肠系膜动脉中一氧化氮生物利用度的降低，而且还抵消了前者中内皮依赖性收缩的增强。
Individual vascular beds exhibit differences in vascular reactivity. The present study investigates the effects of streptozotocin-induced type I diabetes on endothelium-dependent responses of rat carotid, femoral, and mesenteric arteries. Rings with and without endothelium, suspended in organ chambers for isometric tension recording, were contracted with phenylephrine and exposed to increasing concentrations of acetylcholine. In carotid and femoral arteries, acetylcholine produced concentration- and endothelium-dependent relaxations that were abolished by Nω-nitro-l-arginine methyl ester (l-NAME; specific nitric-oxide synthase inhibitor) and were impaired slightly in preparations from streptozotocin-treated rats (STZ-rats). This impairment could be prevented by l-arginine. In femoral arteries incubated with l-NAME, acetylcholine caused endothelium-dependent contractions that were abolished by 3-[(6-amino-(4-chlorobenzensulfonyl)-2-methyl-5,6,7,8-tetrahydronapht]-1-yl) propionic acid (S18886) (antagonist of thromboxane A2/prostaglandins H2-receptors) and reversed to relaxation by indomethacin (inhibitor of cyclooxygenase). The latter relaxation was inhibited by charybdotoxin plus apamin, suggesting a role of endothelium-dependent hyperpolarizing factor (EDHF). This EDHF-mediated component was augmented slightly in arteries from STZ-rats. In mesenteric arteries, relaxations to acetylcholine were only partially inhibited by l-NAME, and the l-NAME-resistant component was abolished by charybdotoxin plus apamin. In the mesenteric arteries from STZ-rats, l-NAME-sensitive relaxations to acetylcholine were reduced and the EDHF-component was augmented. These findings demonstrate a marked heterogeneity in endothelium-dependent responses in rat arteries and their differential adaptation in the course of type I diabetes. In particular, the EDHF-mediated component not only compensates for the reduced bioavailability of nitric oxide in the femoral and mesenteric artery but also counteracts the augmented endothelium-dependent contractions in the former.
cGMP 介导离体犬冠状动脉对缓激肽的脱敏。
DOI：
10.1152/ajpheart.1995.268.2.h865
发表时间：
1995
期刊：
The American journal of physiology.
影响因子：
--
作者：
Olmos,L;Mombouli,JV;Illiano,S;Vanhoutte,PM
通讯作者：
Vanhoutte,PM
影响因子：
8.3
作者：
LUSCHER, TF;VANHOUTTE, PM
通讯作者：
VANHOUTTE, PM
影响因子：
--
作者：
NAGAO, T;ILLIANO, S;VANHOUTTE, PM
通讯作者：
VANHOUTTE, PM