Angiotensin II-induced aortic ring constriction is mediated by phosphatidylinositol 3-kinase/L-type calcium channel signaling pathway
Experimental & Molecular Medicine
;
: 569-576, 2009.
Article
in English
| WPRIM
| ID: wpr-34743
ABSTRACT
Angiotensin II (AngII) is a crucial hormone that affects vasoconstriction and exerts hypertrophic effects on vascular smooth muscle cells. Here, we showed that phosphatidylinositol 3-kinase-dependent calcium mobilization plays pivotal roles in AngII-induced vascular constriction. Stimulation of rat aortic vascular smooth muscle cell (RASMC)-embedded collagen gel with AngII rapidly induced contraction. AngII-induced collagen gel contraction was blocked by pretreatment with a phosphatidylinositol 3-kinase (PI3K) inhibitor (LY294002) whereas ERK inhibitor (PD98059) was not effective. AngII-induced collagen gel contraction was significantly blocked by extracellular calcium depletion by EGTA or by nifedipine which is an L-type calcium channel blocker. In addition, AngII-induced calcium mobilization was also blocked by nifedipine and EGTA, whereas intracellular calcium store-depletion by thapsigargin was not effective. Finally, pretreatment of rat aortic ring with LY294002 and nifedipine significantly reduced AngII-induced constriction. Given these results, we suggest that PI3K-dependent activation of L-type calcium channels might be involved in AngII-induced vascular constriction.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Aorta, Thoracic
/
Vasoconstriction
/
Angiotensin II
/
Signal Transduction
/
Rats, Sprague-Dawley
/
Specific Pathogen-Free Organisms
/
Calcium Channels, L-Type
/
Phosphatidylinositol 3-Kinase
/
Muscle Contraction
/
Muscle, Smooth, Vascular
Limits:
Animals
Language:
English
Journal:
Experimental & Molecular Medicine
Year:
2009
Type:
Article
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