Bleeker W K, Van Rosevelt R F, Ufkes J G, Loos J A, Van Mourik J A, Bakker J C
J Lab Clin Med. 1982 Oct;100(4):540-7.
In a rat model, the relationship between the activity of PKA in human PPFs, the changes in arterial BK concentration, and the changes in blood pressure on infusion of PPF was investigated. The rat was chosen as a model because it is reported to be one of the few animals sensitive to human PKA. However, hypotensive reactions after infusion of human PKA-containing PPF were observed only in the presence of a bradykinin-potentiating peptide (BPP9a). A correlation was found between the PKA content of the rapidly infused PPF, the BK generation in the rat, and the fall in arterial blood pressure. In control experiments, infusions of BK provoKed a similar fall in blood pressure at corresponding BK levels. After neutralization of the PKA activity in the PPF with C1-esterase inhibitor, neither a rise in BK level nor a fall in blood pressure was observed on infusion. We conclude therefore that the hypotensive reactions were caused by PKA-mediated generation of BK.
在大鼠模型中,研究了人腮腺分泌液(PPF)中蛋白激酶A(PKA)的活性、动脉缓激肽(BK)浓度的变化以及输注PPF时血压的变化之间的关系。选择大鼠作为模型是因为据报道它是对人PKA敏感的少数动物之一。然而,仅在存在缓激肽增强肽(BPP9a)的情况下,才观察到输注含人PKA的PPF后的低血压反应。在快速输注的PPF的PKA含量、大鼠体内BK的生成与动脉血压下降之间发现了相关性。在对照实验中,输注BK在相应的BK水平下引起了类似的血压下降。在用C1酯酶抑制剂中和PPF中的PKA活性后,输注时既未观察到BK水平升高,也未观察到血压下降。因此,我们得出结论,低血压反应是由PKA介导的BK生成引起的。