Angiotensin II stimulation of Ca 2+ -channel current in vascular smooth muscle cells is inhibited by lavendustin-A and LY-294002

1999 ◽  
Vol 437 (3) ◽  
pp. 317-323 ◽  
Author(s):  
T. Seki ◽  
Hisashi Yokoshiki ◽  
Masanori Sunagawa ◽  
Mariko Nakamura ◽  
Nicholas Sperelakis
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Channel Current ◽  
Stimulation Of

scholarly journals Constitutive Stimulation of Vascular Smooth Muscle Cells by Angiotensin II Derived From an Adenovirus Encoding a Furin-Cleavable Fusion Protein

2012 ◽  
Vol 25 (3) ◽  
pp. 280-283 ◽  
Author(s):  
Takehiko Takayanagi ◽  
Allison M. Bourne ◽  
Keita Kimura ◽  
Akira Takaguri ◽  
Katherine J. Elliott ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Fusion Protein ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Stimulation Of

Mechanism of angiotensin II stimulation of Na-K-Cl cotransport of vascular smooth muscle cells

1989 ◽  
Vol 257 (4) ◽  
pp. C629-C636 ◽  
Author(s):  
N. E. Owen ◽  
K. M. Ridge
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Intracellular Calcium ◽  
Vascular Smooth Muscle Cells ◽  
Calcium Influx ◽  
Muscle Cells ◽  
Intracellular Calcium Mobilization ◽  
Stimulation Of

Previous studies from this laboratory have demonstrated that Na-K-Cl cotransport of vascular smooth muscle cells is inhibited by hormones that increase intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels (e.g., catecholamines) and is stimulated by hormones that increase intracellular guanosine 3',5'-cyclic monophosphate (cGMP) levels (e.g., atrial natriuretic peptides). Others have suggested that calcium may also modulate Na-K-Cl cotransport of vascular smooth muscle cells. The goal of the present study was to characterize the mechanism of angiotensin II stimulation of Na-K-Cl cotransport of early passage cultured vascular smooth muscle cells. We found that when vascular smooth muscle cells were treated with angiotensin II or a calcium ionophore, Na-K-Cl cotransport was markedly enhanced above basal levels. We found that when calcium influx was blocked with the calcium chelator EDTA or with three different chemical types of calcium-channel blockers, the stimulatory effects of angiotensin II on Na-K-Cl cotransport were markedly inhibited. Furthermore, when intracellular calcium mobilization was blocked with high concentrations of the calcium chelator quin2 or with the intracellular calcium antagonist 8-(diethyl-amino)octyl 3,4,5-trimethoxybenzoate (TMB-8), the stimulatory effects of angiotensin II on Na-K-Cl cotransport were also substantially inhibited. These results suggest that both calcium influx via receptor-operated calcium channels and intracellular calcium mobilization may play a role in stimulation of Na-K-Cl cotransport of vascular smooth muscle cells in response to angiotensin II.

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