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血管紧张素II和血管加压素刺激大鼠系膜细胞中的钙激活氯电导。

Angiotensin II and vasopressin stimulate calcium-activated chloride conductance in rat mesangial cells.

作者信息

Okuda T, Yamashita N, Kurokawa K

出版信息

J Clin Invest. 1986 Dec;78(6):1443-8. doi: 10.1172/JCI112734.

Abstract

In an attempt to clarify the mechanisms by which angiotensin II (AII) and arginine vasopressin (AVP) regulate mesangial cell function, we examined the membrane potential change of mesangial cells and found that cells contracted and membrane potential depolarized in response to AII and AVP. The depolarization was associated with decreased input resistance. Ca ionophore A23187 caused similar mesangial cell contraction and depolarization. The reversal potential (Vr) of the depolarization response to AII and AVP was -29 +/- 3 and -25 +/- 7 mV (mean +/- SD), respectively. Not only the Vr of the AII-induced depolarization but also Vr of the Ca ionophore-induced response was dependent upon the extracellular Cl- concentration. Further, AII and AVP caused cell contraction and membrane depolarization in Ca++-free medium containing 0.5 mM EGTA. These data suggest the presence of Ca++ -activated Cl- channels in the mesangial cells and that AII and AVP increase Cl- permeability via an elevation of [Ca++]i released from the intracellular organellae.

摘要

为了阐明血管紧张素II(AII)和精氨酸加压素(AVP)调节系膜细胞功能的机制,我们检测了系膜细胞的膜电位变化,发现细胞在AII和AVP作用下会收缩且膜电位去极化。这种去极化与输入电阻降低有关。钙离子载体A23187可引起类似的系膜细胞收缩和去极化。对AII和AVP去极化反应的反转电位(Vr)分别为-29±3和-25±7mV(平均值±标准差)。不仅AII诱导的去极化的Vr,而且钙离子载体诱导反应的Vr都依赖于细胞外Cl-浓度。此外,AII和AVP在含有0.5mM EGTA的无Ca++培养基中也会引起细胞收缩和膜去极化。这些数据表明系膜细胞中存在Ca++激活的Cl-通道,并且AII和AVP通过提高从细胞内细胞器释放的[Ca++]i来增加Cl-通透性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50ff/423888/6f41f683f5cb/jcinvest00111-0036-a.jpg

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