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首页> 外文期刊>Life sciences >Pharmacomechanical coupling in rat vas deferens: effects of agents that modulate intracellular release of calcium and protein kinase C activation.
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Pharmacomechanical coupling in rat vas deferens: effects of agents that modulate intracellular release of calcium and protein kinase C activation.

机译：大鼠输精管中的药理耦合：调节钙和蛋白激酶C活化的细胞内释放的药物的作用。

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摘要

The effects of agents that modulate intracellular release of calcium and protein kinase C (PKC) activation on noradrenaline (NA)-induced contractions of epididymal vas deferens in calcium-free/EGTA (1 mM) medium were investigated. NA (100 microM) or methoxamine (100 microM) evoked repeatable contractions. Clonidine (100-300 microM) was ineffective. The contractions to NA were reduced by procaine (1-10 mM) but not by thapsigargin (0.1-30 microM), ryanodine (1-30 microM) or TMB-8 (1-30 microM). Contractions to cumulative additions of NA (1-100 microM) were enhanced in the presence of cyclopiazonic acid (10 & 30 microM) but not ryanodine (10 & 30 microM). Sequential contractions to NA were not blocked by PKC inhibitors, calphostin C (1 microM) or Ro 31-8220 (1-30 microM) but were reduced by H-7 (1-30 microM), a broad spectrum protein kinase inhibitor. Although RT-PCR experiments detected mRNA for some Ca2+-dependent/DAG-activated and Ca2+-independent/DAG-activated PKC isoforms in epididymal vas deferens, the PKC activators, phorbol 12, 13-dibutyrate (100 microM) or phorbol 12-myristate 13-acetate (100 microM) failed to activate the tissues in calcium-free medium but enhanced subsequent contractions to NA. These results indicate a limited role for intracellular calcium stores and phorbol ester/DAG-sensitive PKC isoforms in NA-induced contraction of epididymal rat vas deferens in calcium-free medium. The results suggest that pharmacomechanical coupling triggered by NA may involve the sensitization of contractile myofilaments to Ca2+ or a Ca2+-independent mechanism. The possible involvement of Ca2+-independent/DAG-insensitive PKC isoforms and agonist-dependent but PKC-independent sensitization pathway is discussed.
机译：研究了在无钙/ EGTA（1 mM）培养基中调节钙离子和蛋白激酶C（PKC）活化的细胞内释放剂对去甲肾上腺素（NA）诱导的附睾输精管收缩的影响。 NA（100 microM）或甲氧胺（100 microM）引起可重复的收缩。可乐定（100-300 microM）无效。普鲁卡因（1-10 mM）减少了对NA的收缩，但thapsigargin（0.1-30 microM），ryanodine（1-30 microM）或TMB-8（1-30 microM）却没有。在环吡嗪酸（10＆30 microM）的存在下，NA累积添加量的收缩（1-100 microM）增强，但雷诺丹（10＆30 microM）则没有。 PKC抑制剂，钙磷蛋白C（1 microM）或Ro 31-8220（1-30 microM）不会阻断对NA的顺序收缩，但广谱蛋白激酶抑制剂H-7（1-30 microM）可以减少其顺序收缩。尽管RT-PCR实验在附睾输精管中检测到一些Ca2 +依赖性/ DAG激活和Ca2 +依赖性/ DAG激活的PKC亚型的mRNA，但PKC激活剂，佛波12、13-二丁酸酯（100 microM）或佛豆蔻12-肉豆蔻酸酯13醋酸盐（100 microM）无法激活无钙培养基中的组织，但增强了随后向NA的收缩。这些结果表明细胞内钙存储和佛波酯/ DAG敏感的PKC亚型在无钙培养基中NA诱导的附睾大鼠输精管收缩中的作用有限。结果表明，NA触发的药效耦合可能涉及收缩性肌丝对Ca2 +的敏化或不依赖Ca2 +的机制。讨论了可能与Ca2 +不相关/ DAG不敏感的PKC同工型和激动剂依赖性但PKC独立的致敏途径有关。

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