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蛋白激酶 Cα 和蛋白激酶 Cι 在去氧肾上腺素诱导的大鼠海绵体收缩中的作用

Role of PKCalpha and PKCiota in phenylephrine-induced contraction of rat corpora cavernosa.

作者信息

Husain S, Young D, Wingard C J

机构信息

Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, Georgia 30912, USA.

出版信息

Int J Impot Res. 2004 Aug;16(4):325-33. doi: 10.1038/sj.ijir.3901164.

Abstract

Constriction of the penile vasculature prevents erection and is largely mediated by physiological agonists. We hypothesized that protein kinase C (PKC) may act as a regulator of penile vascular tone. Studies were designed to identify PKC isoforms present and to investigate their roles in phenylephrine-induced muscle contraction in the isolated rat corpora cavernosa. We demonstrated the presence of PKCalpha, beta, gamma, epsilon, delta, eta, and iota in rat corpora cavernosa and a subcellular distribution, which favored a membrane association for PKCalpha, beta, delta, and iota. Phenylephrine (3 microM) generated an active stress of 9.6 +/- 1.5 mN/mm2 and was associated with a significant increase of PKCalpha and PKCiota immunoreactivity in the particulate fraction. The amount of PKCalpha and PKCiota in the particulate fraction rose by 36 +/- 4.4 and 51 +/- 2.2% with phenylephrine stimulation. Furthermore, the phenylephrine concentration-response curve was potentiated in the presence of phorbol 12-myristate13-acetate (PMA) (0.1 microM), a PKC activator (EC50: phenylephrine 1.0 +/- 0.8 microM vs phenylephrine + PMA 0.3 +/- 0.1 microM) and inhibited in the presence of chelerythrine chloride (30 microM), a PKC inhibitor (EC50: phenylephrine 1.0 +/- 0.8 microM vs phenylephrine + chelerythrine chloride 5.7 +/- 2.4 microM). Based on these results, we suggest a potential role for PKCalpha and PKCiota in phenylephrine-induced smooth muscle tone of the rat cavernosum.

摘要

阴茎血管收缩会阻止勃起,且很大程度上由生理性激动剂介导。我们推测蛋白激酶C(PKC)可能作为阴茎血管张力的调节因子。本研究旨在鉴定存在的PKC亚型,并研究它们在去氧肾上腺素诱导的离体大鼠海绵体肌肉收缩中的作用。我们证实在大鼠海绵体中存在PKCα、β、γ、ε、δ、η和ι,且其亚细胞分布显示PKCα、β、δ和ι倾向于与细胞膜结合。去氧肾上腺素(3 microM)产生9.6±1.5 mN/mm2的主动张力,并与颗粒部分中PKCα和PKCι免疫反应性的显著增加相关。去氧肾上腺素刺激后,颗粒部分中PKCα和PKCι的量分别增加了36±4.4%和51±2.2%。此外,在蛋白激酶C激活剂佛波醇12-肉豆蔻酸酯13-乙酸酯(PMA)(0.1 microM)存在的情况下,去氧肾上腺素浓度-反应曲线增强(EC50:去氧肾上腺素1.0±0.8 microM 对比 去氧肾上腺素 + PMA 0.3±0.1 microM),而在蛋白激酶C抑制剂氯化白屈菜红碱(30 microM)存在的情况下受到抑制(EC50:去氧肾上腺素1.0±0.8 microM 对比 去氧肾上腺素 + 氯化白屈菜红碱5.7±2.4 microM)。基于这些结果,我们认为PKCα和PKCι在去氧肾上腺素诱导的大鼠海绵体平滑肌张力中具有潜在作用。

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