Pathways of [Ca2+]i rise evoked by angiotensin II in MDCK renal tubular cells. (December 2013)

• Record Type: Journal Article
• Authors: Liu, Chung-Pin; Chou, Chiang-Ting; Liang, Wei-Zhe; Cheng, Jin-Shiung; Chang, Hong-Tai; Kuo, Daih-Huang; Ko, Kuang-Chung; Chiang, Ni-Na; Wu, Ru-Fang; Shieh, Pochuen; Jan, Chung-Ren
• Is Part Of: Journal of receptor and signal transduction research. Volume 33:Number 6(2013)
• Page Start: 380
• Page End: 386
• Publication Date: 2013-12
• Subjects: Cell receptors -- Periodicals; Cellular signal transduction -- Periodicals; 571.6
• DOI: 10.3109/10799893.2013.838788
• Languages: English
• ISSNs: 1079-9893

Abstract

<abstract> <title>Abstract</title> <p>The effect of angiotensin II (Ang II) on cytosolic Ca²⁺ concentrations ([Ca²⁺]_i) in MDCK renal tubular cells was explored. The Ca²⁺-sensitive fluorescent dye fura-2 was applied to measure [Ca²⁺]_i. Ang II at concentrations of 5–40 µM induced a [Ca²⁺]_i rise in a concentration-dependent manner. The response was reduced partly by removing Ca²⁺. Ang II evoked store-operated Ca²⁺ entry that was inhibited by La³⁺ and Gd³⁺. In the absence of extracellular Ca²⁺, incubation with the endoplasmic reticulum Ca²⁺ pump inhibitor 2, 5-di-tert-butylhydroquinone (BHQ) or thapsigargin abolished Ang II-induced Ca²⁺ release. Inhibition of phospholipase C with U73122 abolished Ang II-induced [Ca²⁺]_i rise. Three Ang II analogues [(ASN1, VAL5)-Ang II acetate, (SAR1, THR8)-Ang II acetate, (VAL5)-Ang II acetate] failed to induce a [Ca²⁺]_i rise. Together, in MDCK cells, Ang II induced a [Ca²⁺]_i rise via Ca²⁺ entry through store-operated Ca²⁺ channels and phospholipase C-dependent Ca²⁺ release from the endoplasmic reticulum. Moreover, Ang II's amino acid sequence is important in its stimulatory effect on [Ca²⁺]_i.</p> </abstract>