ATP Activates the Potassium Channel and Enhances Cytosolic Ca2+ Release via a P2Y Purinoceptor Linked to Pertussis Toxin-Insensitive G-Protein in Brain Artery Endothelial Cells

1995 ◽  
Vol 215 (3) ◽  
pp. 1022-1028 ◽  
Author(s):  
Y. Ikeuchi ◽  
T. Nishizaki
Keyword(s):  
Endothelial Cells ◽  
Potassium Channel ◽  
G Protein ◽  
Pertussis Toxin ◽  
Brain Artery

Adenosine Induces Cl− Efflux in Endothelial Cells via a Pertussis Toxin-Sensitive G Protein

1994 ◽  
Vol 204 (3) ◽  
pp. 1143-1149 ◽  
Author(s):  
M. Arima ◽  
S. Ueda ◽  
S. Matsushita ◽  
T. Ozawa ◽  
H. Yamaguchi
Keyword(s):  
Endothelial Cells ◽  
G Protein ◽  
Pertussis Toxin

Lysophosphatidylcholine modifies G protein-dependent signaling in porcine endothelial cells

1993 ◽  
Vol 264 (3) ◽  
pp. H722-H727 ◽  
Author(s):  
N. A. Flavahan
Keyword(s):  
Endothelial Cells ◽  
G Protein ◽  
Pertussis Toxin ◽  
Oxidized Ldl ◽  
Isometric Tension ◽  
Nitric Oxide Donor ◽  
Physiological Salt Solution ◽  
Gi Protein ◽  
Porcine Endothelial Cells ◽  
Dependent Pathway

Certain endothelial receptors are coupled to a pertussis toxin-sensitive inhibitory guanine nucleotide-binding regulatory (Gi) protein. In pigs, hypercholesterolemia causes a selective impairment of this Gi protein-dependent pathway. Recent studies have suggested that hypercholesterolemia-induced endothelial dysfunction may be caused by lysophosphatidylcholine (LPC) derived from oxidized low-density lipoprotein (LDL). The aim of the present study was to determine whether LPC could inhibit the Gi protein-dependent pathway. Isolated rings of porcine coronary arteries were suspended for isometric tension recording in organ chambers filled with physiological salt solution (37 degrees C, 95% O2-5% CO2). In rings with endothelium contracted with prostaglandin F2 alpha, pertussis toxin (100 ng/ml) or LPC (10(-5) M) inhibited the endothelium-dependent relaxations evoked by UK-14,304, an alpha 2-adrenergic agonist, or by serotonin, but not those caused by bradykinin or ADP. LPC also did not inhibit relaxations produced by SIN 1, an endothelium-derived relaxing factor-nitric oxide donor. After treatment of the rings with pertussis toxin, LPC no longer inhibited the endothelium-dependent relaxations to serotonin. Although LPC inhibited the responses of membrane-bound receptors that activate the pertussis toxin-sensitive Gi protein, LPC did not affect the endothelium-dependent relaxations evoked by direct activation of the pertussis toxin-sensitive Gi protein by fluoride. These results suggest that LPC selectively inhibits a Gi protein-dependent pathway in porcine endothelial cells possibly by disrupting receptor-G protein interactions. LPC that is associated with oxidized LDL may mediate in part the dysfunction in the endothelial Gi protein-dependent pathway associated with hypercholesterolemia.

Analysis of Pertussis Toxin-Sensitive Receptor: G-Protein Interactions in Native Porcine Endothelial Cells

Endothelium ◽  
1995 ◽  
Vol 3 (4) ◽  
pp. 321-330 ◽  
Author(s):  
J. E. Freeman ◽  
W. Y. Kuo ◽  
G. Milligan ◽  
C. J. Lowenstein ◽  
M. A. Levine ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
G Protein ◽  
Pertussis Toxin ◽  
Protein Interactions ◽  
Porcine Endothelial Cells
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