首页> 外文期刊>Hypertension: An Official Journal of the American Heart Association >Immunohistochemical evidence that angiotensins I and II are formed by intracellular mechanism in juxtaglomerular cells.
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Immunohistochemical evidence that angiotensins I and II are formed by intracellular mechanism in juxtaglomerular cells.

机译:免疫组织化学证据表明血管紧张素I和II是由近肾小细胞中的细胞内机制形成的。

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The existence of angiotensin II (AII) immunoreactivity in juxtaglomerular (JG) cells of rat kidney, which has been demonstrated previously by immunohistochemical studies, can be explained either as the product of intracellular synthesis or by the internalization of receptor-bound AII originating in plasma. To resolve these two alternative mechanisms, attempts were made to identify AI in JG cells of rat kidney by immunohistochemical staining using specific antibodies to AI. Although AI-like immunoreactivity was not detected in normal rat kidney, rats treated with the angiotensin-converting enzyme inhibitors, MK-421 or captopril, showed AI-like immunoreactivity in JG cells. The presence of renin and AII-like immunoreactivity was demonstrated in the same cells by specific antibodies to respective antigens used on adjacent serial sections. These findings support an intracellular mechanism of the formation of AII and suggest an intracellular renin angiotensin system, presumably separate from the extracellular system.
机译:先前已通过免疫组织化学研究证实的大鼠肾脏的肾小球(JG)细胞中血管紧张素II(AII)免疫反应性的存在,可以解释为细胞内合成的产物,也可以解释为源自血浆的受体结合AII的内在化。为了解决这两种替代机制,试图通过使用针对AI的特异性抗体的免疫组织化学染色来鉴定大鼠肾脏JG细胞中的AI。尽管在正常的大鼠肾脏中未检测到AI样的免疫反应性,但用血管紧张素转换酶抑制剂MK-421或卡托普利治疗的大鼠在JG细胞中显示出AI样的免疫反应性。肾素和AII样免疫反应性的存在在同一细胞中通过针对相邻序列切片中使用的相应抗原的特异性抗体得以证实。这些发现支持了AII形成的细胞内机制,并暗示了可能与细胞外系统分离的细胞内肾素血管紧张素系统。

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