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Augmented acetylcholine-induced, Rho-mediated Ca2+ sensitization of bronchial smooth muscle contraction in antigen-induced airway hyperresponsive rats

机译:抗原诱导的气道高反应性大鼠中增强的乙酰胆碱诱导的,Rho介导的支气管平滑肌收缩的Ca2 +致敏

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摘要

Treatment with acetylcholine (ACh) of a β-escin-permeabilized intrapulmonary bronchial smooth muscle of the rat induced force when the Ca2+ concentration was clamped at 1 μM. The ACh-induced Ca2+ sensitization of myofilaments was significantly greater in antigen-induced airway hyperresponsive rats than in control rats. The ACh-induced Ca2+ sensitization was completely blocked by treatment with Clostridium botulinum C3 exoenzyme, an inactivator of Rho family of proteins. Moreover, the protein level of RhoA in the intrapulmonary bronchi was significantly increased in the airway hyperresponsive rats. Thus, increased airway smooth muscle contractility observed in asthmatics may be related to augmented agonist-induced, Rho-mediated Ca2+ sensitization of myofilaments.
机译:当Ca2 +浓度固定在1μM时,用乙酰胆碱(ACh)处理大鼠的β-七叶桃通透性肺内支气管平滑肌。在抗原诱导的气道高反应性大鼠中,ACh诱导的肌丝Ca2 +敏化程度明显高于对照组。 ACh诱导的Ca2 +致敏作用可以通过肉毒梭状芽胞杆菌C3外切酶(一种Rho蛋白家族的失活剂)进行完全阻断。此外,在气道高反应性大鼠中,肺内支气管中RhoA的蛋白质水平显着增加。因此,在哮喘患者中观察到的气道平滑肌收缩力增加可能与激动剂诱导的,Rho介导的肌丝Ca2 +敏化增强有关。

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