Extracellular acidosis suppresses endothelial function by inhibiting store-operated Ca2+ entry via non-selective cation channels

Cardiovascular Research

Volumn 83, Issue 1, 2009, Pages 97-105

  Asai, Masayoshi ^a   Takeuchi, Kazuhiko ^a   Saotome, Masao ^a   Urushida, Tsuyoshi ^a   Katoh, Hideki ^a   Satoh, Hiroshi ^a   Hayashi, Hideharu ^a   Watanabe, Hiroshi ^a  

^a HAMAMATSU UNIVERSITY SCHOOL OF MEDICINE   (Japan)

Author keywords

Acidosis; Endothelial cells; NO; PGI2; Store operated calcium entry

Indexed keywords

6 OXOPROSTAGLANDIN F1 ALPHA; BRADYKININ; CALCIUM ION; CATION CHANNEL; ENDOTHELIUM DERIVED RELAXING FACTOR; FURA 2; NITRIC OXIDE; PROPIONIC ACID; PROSTACYCLIN; THAPSIGARGIN;

ACIDOSIS; ANIMAL CELL; ARTICLE; CALCIUM TRANSPORT; CELL PH; CONTROLLED STUDY; EXTRACELLULAR MATRIX; FLUOROMETRY; NONHUMAN; PRIORITY JOURNAL; VASCULAR ENDOTHELIUM;

ACIDOSIS; ANIMALS; AORTA; BRADYKININ; CALCIUM; CELLS, CULTURED; DISEASE MODELS, ANIMAL; ENDOTHELIUM, VASCULAR; ENDOTHELIUM-DEPENDENT RELAXING FACTORS; EPOPROSTENOL; HYDROGEN-ION CONCENTRATION; ION CHANNELS; NITRIC OXIDE; SWINE; THAPSIGARGIN;

EID: 67649373931     PISSN: 00086363     EISSN: 17553245     Source Type: Journal    
DOI: 10.1093/cvr/cvp105     Document Type: Article

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