The effects of captopril, an angiotensin-converting enzyme inhibitor (ACEI), and a selective B2 kinin receptor antagonist (Icatibant) were examined on the paw edema and tissue contents of bradykinin (BK) and des[Arg9]BK following the intraplantar injection of carrageenan in rats. To this end, BK-like immunoreactivity (BK-LI) and des[Arg9]BK-LI were measured with highly sensitive and specific chemiluminescent enzyme immunoassays. Because pentobarbital significantly reduced the carrageenan-induced edema between 3 and 8 h, experiments were conducted in conscious rats. Icatibant (32.5 nmol/paw; intraplantar) significantly reduced carrageenan-induced paw edema between 3 and 8 h in captopril-untreated rats and at 1 and 3 h in captopril-treated rats (0.2 mg/kg x 5 days, per os). The paw content of BK-LI was increased 10-fold in captopril-untreated and 29-fold in captopril-treated rats 1 h after carrageenan injection. In parallel, des[Arg9]BK-LI was increased 8-fold in captopril-untreated and 24-fold in captopril-treated rats. Icatibant prevented the maximal increases in BK-LI and des[Arg9]BK-LI induced by carrageenan. It is concluded that inhibition of ACE by captopril enhanced the early production of endogenous BK and the edema formation induced by carrageenan through a B2 receptor-mediated mechanism. However, the B2 receptor does not appear to be involved in the late phase of the inflammatory response (from 5 to 24 h) to carrageenan in rats pretreated with ACEI. Although the concentrations of des[Arg9]BK were greater than those of BK, it is unlikely that B1 receptors play a significant role in this model of carrageenan-induced edema.

译文

足底注射异丙酚后,检查了卡托普利,血管紧张素转换酶抑制剂(ACEI)和选择性B2激肽受体拮抗剂(Icatibant)对爪水肿和缓激肽(BK)和des [Arg9] BK的组织含量的影响。大鼠中的角叉菜胶。为此,用高灵敏度和特异性的化学发光酶免疫测定法测量了BK样免疫反应性(BK-LI)和des [Arg9] BK-LI。由于戊巴比妥可在3至8小时内显着减少角叉菜胶引起的水肿,因此在有意识的大鼠中进行了实验。伊卡替班(32.5 nmol /爪;足底内)在未经卡托普利治疗的大鼠中3至8小时以及经卡托普利治疗的大鼠1至3小时内均显着减少了角叉菜胶诱导的爪水肿(0.2 mg / kg x 5天,每次口服)。角叉菜胶注射后1小时,未经卡托普利治疗的大鼠的BK-LI的爪子含量增加10倍,而经卡托普利治疗的大鼠的BK-LI的爪子含量增加29倍。平行地,在未经卡托普利治疗的大鼠中,des [Arg9] BK-LI增加了8倍,而在经卡托普利治疗的大鼠中,des [Arg9] BK-LI增加了24倍。伊卡替班预防了由角叉菜胶诱导的BK-LI和des [Arg9] BK-LI的最大增加。结论是,卡托普利对ACE的抑制作用通过B2受体介导的机制增强了内源性BK的早期产生和角叉菜胶诱导的水肿形成。但是,在用ACEI预处理的大鼠中,B2受体似乎不参与对角叉菜胶的炎症反应的后期(5至24小时)。尽管des [Arg9] BK的浓度高于BK的浓度,但B1受体不太可能在这种由角叉菜胶诱发的水肿模型中发挥重要作用。

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