Kinase activation and smooth muscle contraction in the presence and absence of calcium.
Kinase activation and smooth muscle contraction in the presence and absence of calcium.
复制标题
在钙存在和不存在的情况下激酶激活和平滑肌收缩。
DOI：
10.1016/s0741-5214(95)70086-2
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发表时间：
1995
影响因子：
4.3
通讯作者：
Brophy,C
中科院分区：
文献类型：
--
作者：
Whitney,G;Throckmorton,D;Isales,C;Takuwa,Y;Yeh,J;Rasmussen,H;Brophy,C
目的调控血管痉挛时血管平滑肌持续收缩的细胞内信号传导机制尚不清楚。本研究的目的是研究细胞信号传导机制，解释持续的血管平滑肌收缩，独立于细胞内Ca2+浓度（[Ca2+]i）的增加。方法用肌浴法观察新鲜牛颈动脉平滑肌的收缩反应。[Ca2+]通过使用细胞外Ca2+螯合剂乙二醇-双（ß-氨基乙醚）N，N,N ',N ' -四乙酸和细胞内螯合剂1,2-双（2-氨基苯氧基）乙烷-N，N,N ',N '，-四乙酸来消耗。结果在无Ca2+条件下，高KCI的膜去极化不能引起收缩。此外，通过Ca2+指示剂Fura 2测定，在无Ca2+条件下，（[Ca2+]i）小于10 nmol/L。蛋白激酶C （PKC）激活剂phorbol 12,13 -二丁酸酯（PDBu）在牛颈动脉平滑肌中诱导缓慢持续的收缩，且在Ca2+存在和不存在的情况下，对PDBu （10 μmol/L ~ 10 μmol/L）的收缩反应幅度相同。肌球蛋白轻链激酶抑制剂ML-9 （50 μmol/L）不抑制PDBu在Ca2+游离条件下的收缩，但PKC抑制剂staurosporine （50 nmol/L）可抑制PDBu的收缩。结论血管平滑肌在Ca2+水平较低且固定的情况下可发生收缩，而这些收缩可能是由PKC介导的。（中华外科杂志1995；22:37-44）
PurposeThe intracellular signalling mechanisms that modulate the sustained vascular smooth muscle contractions that occur with vasospasm are not well understood. The purpose of this investigation was to examine cell signalling mechanisms that account for sustained vascular smooth muscle contraction, independent of increases in intracellular Ca2+concentrations ([Ca2+]i).MethodsFresh bovine carotid artery smooth muscles contractile responses were examined in a muscle bath. [Ca2+]iwas depleted by use of the extracellular Ca2+chelator, ethylene glycol-bis(ß-aminoethylether) N, N, N′, N′-tetraacetic acid and the intracellular chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′,-tetraacetic acid.ResultsIn Ca2+-free conditions, depolarizing the membrane with high extracellular KCI failed to elicit a contraction. In addition, in Ca2+-free conditions the ([Ca2+]i) was less than 10 nmol/L as determined with the Ca2+-indicator, Fura 2. The protein kinase C (PKC) activator, phorbol 12, 13-dibutyrate (PDBu), induced slowly developing sustained contractions in bovine carotid artery smooth muscle, and the magnitude of the contractile response to PDBu (10 nmol/L to 10 μmol/L) was the same in the presence and absence of Ca2+. PDBu induced contractions in Ca2+-free conditions were not inhibited by the myosin light chain kinase inhibitor, ML-9 (50 μmol/L), but were inhibited by the PKC inhibitor, staurosporine (50 nmol/L).ConclusionsThese data suggest that vascular smooth muscle contractions can occur under conditions where the [Ca2+]iis low and fixed and that these contractions may be mediated by PKC. (J VASC SURG 1995;22:37-44.)
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DOI：
--
发表时间：
1987
期刊：
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影响因子：
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10.1016/s0021-9258(18)66923-6
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影响因子：
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Katsuyama,H;Morgan,KG
通讯作者：
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DOI：
--
发表时间：
1985-03
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影响因子：
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