The role of myoendothelial cell contact in non‐nitric oxide‐, non‐prostanoid‐mediated endothelium‐dependent relaxation of porcine coronary artery

The role of myoendothelial cell contact in non‐nitric oxide‐, non‐prostanoid‐mediated endothelium‐dependent relaxation of porcine coronary artery
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肌内皮细胞接触在非一氧化氮、非前列腺素介导的猪冠状动脉内皮依赖性舒张中的作用

DOI:
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发表时间:
1994
影响因子:
7.3
通讯作者:
F. Brunner
F. Brunner
中科院分区:
医学2区
文献类型:
--
作者:
E. Kühberger;K. Groschner;W. Kukovetz;F. Brunner

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1实验旨在分析猪冠状动脉中缓激肽诱导的内皮依赖性舒张对NG-硝基-L-精氨酸(L-NOARG)和吲哚美辛的抵抗对肌内皮连接的需求。2用血栓素受体激动剂U46619收缩猪冠状动脉环,并等长记录缓激肽舒张。所有实验均在吲哚美辛存在下进行。NO合成酶抑制剂L-NOARG(250 μm)可阻断一氧化氮(NO)介导的效应,含D-甘露醇或蔗糖(各180 μm)或差距连接解偶联剂1-庚醇(2 μm)的高渗溶液可抑制肌内皮接触。高[K+]溶液(40 μm)用于探测内皮源性超极化因子(EDHF)的可能贡献。3在内皮存在的情况下,缓激肽诱导浓度依赖性舒张,平均EC 50为3.2 nm,最大反应为罂粟碱诱导舒张的95 ± 1%(对照曲线)。4在内皮缺失的情况下,缓激肽不能引起舒张。在器官浴中加入培养的猪主动脉内皮细胞,可使血管松弛,并部分恢复缓激肽的舒张作用。这种内皮细胞介导的舒张作用在250 μm L-NOARG存在下完全消除。5. L-NOARG仅轻微抑制内皮保留环中缓激肽诱导的舒张(对照的86%)。在高细胞外[K+](40 μm)部分去极化的血管中,舒张降低至对照的72%。在存在L-NOARG的情况下,缓激肽未能舒张部分去极化血管。6在存在2 mM 1-庚醇、180 mM甘露醇或180 mM蔗糖的情况下,缓激肽的最大松弛降低至约70%,即与存在高[K+]的情况下相同的程度。剩余的舒张对L-NOARG的阻断敏感。7缓激肽(300 nm)使反映NO活性的组织环GMP含量增加约4倍。这种增加不受高[K+]、庚醇或蔗糖的影响,但被L-NOARG阻断。8我们的结果表明,非一氧化氮和非前列腺素介导的猪冠状动脉内皮依赖性舒张需要功能完整的肌内皮连接。
1 Experiments were designed to analyse the requirement of myoendothelial junctions by bradykinin‐induced endothelium‐dependent relaxations resistant to NG‐nitro‐L‐arginine (L‐NOARG) and indo‐methacin in porcine coronary arteries. 2 Rings of porcine coronary arteries were contracted with the thromboxane receptor agonist, U46619 and relaxations to bradykinin recorded isometrically. All experiments were performed in the presence of indomethacin. Nitric oxide (NO)‐mediated effects were blocked by the NO synthase inhibitor L‐NOARG (250 μm) and myoendothelial contacts inhibited by treatment with hypertonic solution containing D‐mannitol or sucrose (each 180 μm) or the gap junctional uncoupling agent 1‐heptanol (2 μm). High [K+] solutions (40 μm) were used to probe a possible contribution of endothelium‐derived hyperpolarizing factor (EDHF). 3 In the presence of endothelium, bradykinin induced concentration‐dependent relaxations with a mean EC50 of 3.2 nm and a maximum response of 95 ± 1% of papaverine‐induced relaxation (control curve). 4 In the absence of endothelium, bradykinin failed to induce relaxations. Addition of cultured porcine aortic endothelial cells to the organ bath resulted in some relaxation and restored in part the relaxant effect of bradykinin. This endothelial cell‐mediated relaxant effect was completely abolished in the presence of 250 μm L‐NOARG. 5 Bradykinin‐induced relaxations in endothelium‐preserved rings were only slightly suppressed by L‐NOARG (86% of control). In vessels partially depolarized by high extracellular [K+] (40 μm) relaxation was reduced to 72% of control. In the presence of L‐NOARG, bradykinin failed to relax partially depolarized vessels. 6 In the presence of 2 mm 1‐heptanol, 180mM mannitol or 180mM sucrose maximum relaxation to bradykinin was reduced to ∼70%, i.e. to the same extent as in the presence of high [K+]. The remaining relaxation was sensitive to blockade by L‐NOARG. 7 Tissue cyclic GMP content which reflects NO activity, was increased about 4 fold by bradykinin (300 nm). This increase was unaffected by high [K+], heptanol or sucrose but blocked by L‐NOARG. 8 Our results suggest that non‐nitric oxide‐ and non‐prostanoid‐mediated endothelium‐dependent relaxation of porcine coronary artery requires functionally intact myoendothelial junctions.
DOI: 10.1152/ajpcell.1992.263.2.c373
发表时间: 1992-08-01
影响因子: --
作者:
CHRIST, GJ;MORENO, AP;SPRAY, DC
通讯作者: SPRAY, DC
DOI: 10.1152/ajpheart.1990.259.3.h668
发表时间: 1990-09-01
影响因子: --
作者:
BRAYDEN, JE
通讯作者: BRAYDEN, JE
一氧化氮、乙酰胆碱以及犬动脉平滑肌的电学和机械特性。
DOI: 10.1152/ajpheart.1988.255.1.h207
发表时间: 1988
期刊: The American journal of physiology
影响因子: --
作者:
Komori,K;Lorenz,RR;Vanhoutte,PM
通讯作者: Vanhoutte,PM
内皮细胞和平滑肌细胞单层之间的可逆微载体介导的连接通讯:血管细胞相互作用的体外模型。
DOI: --
发表时间: 1985
期刊: Laboratory investigation; a journal of technical methods and pathology
影响因子: --
作者:
Davies,PF;Ganz,P;Diehl,PS
通讯作者: Diehl,PS