A role for inositol 1,4,5‐trisphosphate in the initiation of agonist‐induced contractions of dog tracheal smooth muscle
A role for inositol 1,4,5‐trisphosphate in the initiation of agonist‐induced contractions of dog tracheal smooth muscle
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肌醇 1,4,5-三磷酸在引发激动剂诱导的狗气管平滑肌收缩中的作用
DOI：
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发表时间：
1985
影响因子：
7.3
通讯作者：
Y. Ito
中科院分区：
文献类型：
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作者：
T. Hashimoto;M. Hirata;Y. Ito
1为了阐明1，4，5-三磷酸肌醇（Ins-P3）在激动剂诱导的犬气管平滑肌细胞收缩中的作用，我们研究了乙酰胆碱（ACh）对Ins-P3、磷脂酰肌醇-4，5-二磷酸（PI-P2）或磷脂酸（PA）浓度的影响。还在皂苷透化的平滑肌细胞中研究了Ins-P3对平滑肌细胞中储存的Ca 2+的影响。[2]在游离Ca 2+浓度分别为4.6 × 10−7或5 × 10−5 M的皂苷处理的分散的单个平滑肌细胞中，观察到细胞中Ca 2+的半数最大或最大蓄积。ATP依赖性Ca 2+蓄积最大，为0.63 nmol/105个细胞。3在游离Ca 2+浓度为3.7 × 10−7 M时观察到Ins-P3对储存的Ca 2+的影响，这诱导了约一半的最大ATP依赖性Ca 2+蓄积。Ins-P3以剂量依赖性方式释放ATP积累的Ca 2+。在施加3 μM Ins-P3后，释放了约40%的总Ca 2+。4通过应用Ins-P3诱导的储存的Ca 2+的释放之后，其被再摄取到平滑肌细胞中。因此，随着Ins-P3的重复应用，储存的Ca 2+被重复释放。5将ACh（10 - 5 M）应用于犬气管刺激可溶性部分中Ins-P3的产生，并且在此应用后10 s，Ins-P3的相对量为对照值的290%。6同时，ACh（10 - 5 M）使平滑肌细胞脂质部分中磷脂酰肌醇4，5-二磷酸（PI-P2）或磷脂酸（PA）的含量分别减少或增加至对照值的60%或350%，从而表明ACh刺激PI-P2的磷酸二酯水解。7 5-羟色胺（5-HT; 10−5 M）也使PI-P2或PA的含量分别降低或增加至对照值的80或200%。然而，在存在或不存在西咪替丁（10 − 5 M）的情况下，组胺（10 −5 M）和前列腺素F2α（PGF 2 α 10−7 M）均未对平滑肌细胞脂质组分中PI-P2或PA的含量产生任何影响。8这些结果表明，在狗气管的肌细胞中，Ins-P3可能在ACh或5-HT诱导的收缩的起始中发挥细胞内第二信使的作用，但在组胺或PGF 2 α诱导的收缩中不起作用。
1 To elucidate the role of inositol 1,4,5‐trisphosphate (Ins‐P3) in the initiation of agonist‐induced contraction of the smooth muscle cells of the dog trachea, we investigated the effects of acetylcholine (ACh) on the concentrations of Ins‐P3, phosphatidylinositol‐4,5‐bisphosphate (PI‐P2) or phosphatidic acid (PA). The effects of Ins‐P3 on the Ca2+ stored in the smooth muscle cells were also studied in saponin‐permeabilized smooth muscle cells. 2 A half maximal or maximal Ca2+ accumulation into the cells was observed in the dispersed single, smooth muscle cells treated by saponin, in free Ca2+ concentrations of 4.6 × 10−7 or 5 × 10−5 M, respectively. The ATP‐dependent Ca2+ accumulation was maximal at 0.63 nmol/105 cells. 3 Effects of Ins‐P3 on stored Ca2+ were observed at a free Ca2+ concentration of 3.7 × 10−7 M, which induces about half maximal ATP‐dependent Ca2+‐accumulation. Ins‐P3 released the Ca2+ accumulated by ATP, in a dose‐dependent manner. About 40% of the total Ca2+ was released following application of 3 μM Ins‐P3. 4 The release of stored Ca2+ induced by application of Ins‐P3 was followed by its re‐uptake into the smooth muscle cells. Thus, the stored Ca2+ was repeatedly released with repetitive applications of Ins‐P3. 5 Application of ACh (10−5 M) to the dog trachea stimulated the production of Ins‐P3 in the soluble fraction and 10 s after this application, the relative amount of Ins‐P3 was 290% of the control value. 6 Concomitantly, ACh (10−5 M) either reduced or increased the contents of phosphatidyl inositol 4,5‐biphosphate (PI‐P2) or phosphatidic acid (PA) in the lipid fraction of the smooth muscle cells to 60% or to 350% of the control value, respectively, thereby indicating that ACh stimulates the phosphodiesteric hydrolysis of PI‐P2. 7 5‐Hydroxytryptamine (5‐HT; 10−5 M) also reduced or increased the contents of PI‐P2 or PA to 80 or to 200% of the control values, respectively. However, neither histamine (10−5 M), in the presence or absence of cimetidine (10−5 M), nor prostaglandin F2α (PGF2α 10−7 M) showed any effect on the contents of PI‐P2 or PA in the lipid fraction of the smooth muscle cells. 8 These results indicate that in muscle cells of the dog trachea, Ins‐P3 may play the role of intracellular second messenger in the initiation of ACh or 5‐HT‐induced contraction, but not in the case of histamine or PGF2α‐induced contraction.
肌醇 1,4,5-三磷酸。
DOI：
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发表时间：
1984
期刊：
The Journal of biological chemistry
影响因子：
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作者：
Joseph,SK;Thomas,AP;Williams,RJ;Irvine,RF;Williamson,JR
通讯作者：
Williamson,JR
DOI：
10.1073/pnas.81.21.6899
发表时间：
1984-01-01
期刊：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子：
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作者：
BARON, CB;CUNNINGHAM, M;COBURN, RF
通讯作者：
COBURN, RF
兔虹膜平滑肌中乙酰胆碱刺激的磷脂酰肌醇 4,5-二磷酸酯的磷酸二酯裂解对钙离子的需求。
DOI：
10.1042/bj1920783
发表时间：
1980
期刊：
The Biochemical journal
影响因子：
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作者：
Akhtar,RA;Abdel-Latif,AA
通讯作者：
Abdel-Latif,AA