Protein kinase Cepsilon and the antiadrenergic action of adenosine in rat ventricular myocytes.

Protein kinase Cepsilon and the antiadrenergic action of adenosine in rat ventricular myocytes.
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蛋白激酶 Cepsilon 和腺苷在大鼠心室肌细胞中的抗肾上腺素作用。

DOI:
10.1152/ajpheart.00224.2004
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发表时间:
2004
期刊:
American journal of physiology. Heart and circulatory physiology
影响因子:
--
通讯作者:
DobsonJr,JamesG
DobsonJr,JamesG
中科院分区:
--
文献类型:
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作者:
Miyazaki,Koji;Komatsu,Satoshi;Ikebe,Mitsuo;Fenton,RichardA;DobsonJr,JamesG

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相似文献

腺苷诱导的心脏抗肾上腺素能作用由腺苷a1受体(A1R)介导。以PKCε过表达的成年大鼠心室肌细胞为实验对象,探讨PKCε在腺苷抗肾上腺素能作用中的作用。用pEGFP-N1载体转染存在或不存在PKCε构建体的肌细胞,并与正常肌细胞进行比较。通过视频成像记录静息正常和转染的肌细胞电刺激引起的肌细胞缩短的程度。PKCε主要定位于横小管。1 μM的A1R激动剂氯环戊基腺苷(CCPA)增强了PKCε在t管系统中的定位。β-肾上腺素能激动剂异丙肾上腺素(Iso; 0.4 μM)在所有三组中均引起29-36%的心肌细胞缩短增加。尽管CCPA在所有三组中显著降低了iso产生的缩短增加,但CCPA引起的减少在PKCε过表达时最大。在PKCε抑制肽存在的情况下,CCPA对iso诱导的缩短的减少被消除。这些结果表明PKCε易位到t管系统在心脏a1r介导的抗肾上腺素能作用中起重要作用。
Adenosine-induced antiadrenergic effects in the heart are mediated by adenosine A1receptors (A1R). The role of PKCε in the antiadrenergic action of adenosine was explored with adult rat ventricular myocytes in which PKCε was overexpressed. Myocytes were transfected with a pEGFP-N1 vector in the presence or absence of a PKCε construct and compared with normal myocytes. The extent of myocyte shortening elicited by electrical stimulation of quiescent normal and transfected myocytes was recorded with video imaging. PKCε was found localized primarily in transverse tubules. The A1R agonist chlorocyclopentyladenosine (CCPA) at 1 μM rendered an enhanced localization of PKCε in the t-tubular system. The β-adrenergic agonist isoproterenol (Iso; 0.4 μM) elicited a 29–36% increase in myocyte shortening in all three groups. Although CCPA significantly reduced the Iso-produced increase in shortening in all three groups, the reduction caused by CCPA was greatest with PKCε overexpression. The CCPA reduction of the Iso-elicited shortening was eliminated in the presence of a PKCε inhibitory peptide. These results suggest that the translocation of PKCε to the t-tubular system plays an important role in A1R-mediated antiadrenergic actions in the heart.