Stojic D
Department of Pharmacology, Faculty of Stomatology, University of Belgrade, Yugoslavia.
Eur J Oral Sci. 1999 Feb;107(1):21-4. doi: 10.1046/j.0909-8836.1999.eos107105.x.
The effects of captopril and bradykinin on chorda tympani-induced salivation were studied in the submandibular gland of anesthetized cat. Captopril and bradykinin, but not des-Arg9-bradykinin, increased salivation evoked by electrical stimulation of chorda tympani. These potentiated effects of captopril and bradykinin were suppressed by Hoe-140, a kinin B2 receptor antagonist, or by concomitant addition of N(G)-nitro arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, and aspirin, a cyclooxygenase inhibitor. It appears that captopril potentiates chorda tympani-induced salivation through endogenously accumulated bradykinin, which acts on kinin B2 receptors, mediating production of nitric oxide and cyclooxygenase products.
在麻醉猫的下颌下腺中研究了卡托普利和缓激肽对鼓索神经诱发唾液分泌的影响。卡托普利和缓激肽可增加鼓索神经电刺激诱发的唾液分泌,但去-精氨酸9-缓激肽则无此作用。缓激肽B2受体拮抗剂Hoe-140,或同时添加一氧化氮合酶抑制剂N(G)-硝基精氨酸甲酯(L-NAME)和环氧化酶抑制剂阿司匹林,均可抑制卡托普利和缓激肽的这些增强作用。卡托普利似乎是通过内源性积聚的缓激肽增强鼓索神经诱发的唾液分泌,缓激肽作用于缓激肽B2受体,介导一氧化氮和环氧化酶产物的生成。