Saito Y, Kato M, Kobayashi I, Tatemoto K
Department of Laboratory Medicine, School of Medicine, Gunma University, Maebashi, Japan.
Life Sci. 1996;58(18):1569-74. doi: 10.1016/0024-3205(96)00131-2.
We examined the effects of bradykinin (BK) on the intracellular free calcium concentration ([Ca2+]i) in rat pancreatic acinar AR42J cells. BK induced a dose-dependent rise in [Ca+2]i in AR42J cells between the concentrations of 10(-12)M and 10(-7)M. The BK-evoked response was not affected by the presence of Co2+ or the absence of extracellular calcium. This response was suppressed by neomycin or the B2 antagonist, but not by the B1 antagonist. The response was also attenuated by treatment with dexamethasone. These results suggest that BK increases [Ca2+]i through the B2 receptors by promoting the phosphatidyl inositol turn-over and that, in the process of azaserine-induced undifferentiation, the pancreatic acinar cells strongly express the BK receptors.
我们研究了缓激肽（BK）对大鼠胰腺腺泡AR42J细胞内游离钙浓度（[Ca2+]i）的影响。在10（-12）M至10（-7）M的浓度范围内，BK诱导AR42J细胞内[Ca+2]i呈剂量依赖性升高。BK引发的反应不受Co2+存在与否或细胞外钙缺失的影响。新霉素或B2拮抗剂可抑制该反应，但B1拮抗剂则无此作用。地塞米松处理也可使该反应减弱。这些结果表明，BK通过促进磷脂酰肌醇周转，经由B2受体增加[Ca2+]i，并且在氮杂丝氨酸诱导的去分化过程中，胰腺腺泡细胞强烈表达BK受体。
