Pathways of [Ca²⁺]i rise evoked by angiotensin II in MDCK renal tubular cells.
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 La²⁺ 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.
Department of Internal Medicine, Yuan's General Hospital , Kaohsiung , Taiwan .
Chung-Pin
CP
Liu
Chiang-Ting
CT
Chou
Wei-Zhe
WZ
Liang
Jin-Shiung
JS
Cheng
Hong-Tai
HT
Chang
Daih-Huang
DH
Kuo
Kuang-Chung
KC
Ko
Ni-Na
NN
Chiang
Ru-Fang
RF
Wu
Pochuen
P
Shieh
Chung-Ren
CR
Jan
D000804:Angiotensin II / Q000378:metabolism / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects*; D003600:Cytosol / Q000187:drug effects; D004285:Dogs; D007684:Kidney Tubules / Q000166:cytology / Q000378:metabolism*; D061985:Madin Darby Canine Kidney Cells; D010738:Type C Phospholipases / Q000378:metabolism
D000804:Angiotensin II; D010738:Type C Phospholipases; D002118:Calcium