Inhibition of adenylate-cyclase-coupled G protein complex by ototoxic diuretics andcis-platinum in the inner ear of the guinea pig

1991 ◽  
Vol 248 (8) ◽  
pp. 459-464 ◽  
Author(s):  
T. Koch ◽  
B. Gloddek
Keyword(s):  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Inner Ear ◽  
G Protein ◽  
Protein Complex

Vasopressin and isoproterenol activate adenylate cyclase in the guinea pig inner ear

1979 ◽  
Vol 222 (4) ◽  
pp. 275-283 ◽  
Author(s):  
Hans -Peter Zenner ◽  
Birgit Zenner
Keyword(s):  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Inner Ear

Nonopioid effects of β-casomorphin-5 in guinea pig heart: Alterations to the β-adrenoceptor-G-protein complex and inhibition of myocardial responses to isoproterenol

Peptides ◽  
1991 ◽  
Vol 12 (2) ◽  
pp. 265-270 ◽  
Author(s):  
C. Liebmann ◽  
P. Mentz ◽  
M. Schnittler ◽  
U. Schrader ◽  
K. Neubert ◽  
...  
Keyword(s):  
Guinea Pig ◽  
G Protein ◽  
Protein Complex ◽  
Guinea Pig Heart

Hair Cell Damage in the Inner Ear of the Guinea Pig Due to Noise in a Workshop

1987 ◽  
Vol 103 (5) ◽  
pp. 204-211 ◽  
Author(s):  
B. Erlandsson ◽  
H. Hakanson ◽  
A. Ivarsson ◽  
P. Nilsson ◽  
J. Wersall
Keyword(s):  
Guinea Pig ◽  
Hair Cell ◽  
Inner Ear ◽  
Cell Damage ◽  
Hair Cell Damage

scholarly journals Cryo-EM structure of an activated GPCR–G protein complex in lipid nanodiscs

2021 ◽  
Vol 28 (3) ◽  
pp. 258-267 ◽  
Author(s):  
Meng Zhang ◽  
Miao Gui ◽  
Zi-Fu Wang ◽  
Christoph Gorgulla ◽  
James J. Yu ◽  
...  
Keyword(s):  
G Protein ◽  
Protein Complex ◽  
Lipid Nanodiscs

scholarly journals Involvement of A pertussis Toxin Sensitive G-Protein in the Inhibition of Inwardly Rectifying K+Currents by Platelet-Activating Factor in Guinea-Pig Atrial Cardiomyocytes

1994 ◽  
Vol 3 (1) ◽  
pp. 45-51
Author(s):  
M. Gollasch ◽  
T. Kleppisch ◽  
D. Krautwurst ◽  
D. Lewinsohn ◽  
J. Hescheler
Keyword(s):  
Cyclic Amp ◽  
Guinea Pig ◽  
G Protein ◽  
Pertussis Toxin ◽  
Platelet Activating Factor ◽  
Resting Membrane Potential ◽  
Patch Clamp Technique ◽  
Guinea Pig Heart ◽  
Ventricular Cells ◽  
Inwardly Rectifying

Platelet-activating factor (PAF) inhibits single inwardly rectifying K+channels in guinea-pig ventricular cells. There is currently little information as to the mechanism by which these channels are modulated. The effect of PAF on quasi steady-state inwardly rectifying K+currents (presumably of the IK1type) of auricular, atrial and ventricular cardiomyocytes from guinea-pig were studied. Applying the patch-clamp technique in the whole-cell configuration, PAF (10 nM) reduced the K+currents in all three cell types. The inhibitory effect of PAF occurred within seconds and was reversible upon wash-out. It was almost completely abolished by the PAF receptor antagonist BN 50730. Intracellular infusion of atrial cells with guanine 5′-(β-thio)diphosphate (GDPS) or pretreatment of cells with pertussis toxin abolished the PAF dependent reduction of the currents. Neither extracellularly applied isoproterenol nor intracellularly applied adenosine 3′,5′-cyclic monophosphate (cyclic AMP) attenuated the PAF effect. In multicellular preparations of auricles, PAF (10 nM) induced arrhythmias. The arrhythmogenic activity was also reduced by BN 50730. The data indicate that activated PAF receptors inhibit inwardly rectifying K+currents via a pertussis toxin sensitive G-protein without involvement of a cyclic AMP-dependent step. Since IK1is a major component in stabilizing the resting membrane potential, the observed inhibition of this type of channel could play an important role in PAF dependent arrhythmogenesis in guinea-pig heart.

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