scholarly journals Endothelin activates voltage-dependent Ca2+ current by a G protein-dependent mechanism in rabbit cardiac myocytes.

1992 ◽  
Vol 448 (1) ◽  
pp. 729-747 ◽  
Author(s):  
M R Lauer ◽  
M D Gunn ◽  
W T Clusin
Keyword(s):  
G Protein ◽  
Cardiac Myocytes ◽  
Voltage Dependent ◽  
Dependent Mechanism

scholarly journals Intracellular Na+inhibits voltage-dependent N-type Ca2+channels by a G protein βγ subunit-dependent mechanism

2004 ◽  
Vol 556 (1) ◽  
pp. 121-134 ◽  
Author(s):  
Yakov Blumenstein ◽  
Olexandr P. Maximyuk ◽  
Natalia Lozovaya ◽  
Natalia M. Yatsenko ◽  
Nataly Kanevsky ◽  
...  
Keyword(s):  
G Protein ◽  
Voltage Dependent ◽  
Ca2 Channels ◽  
Dependent Mechanism

Reciprocal inhibition of voltage-gated potassium currents (IK(V)) by activation of cannabinoid CB1and dopamine D1receptors in ON bipolar cells of goldfish retina

2005 ◽  
Vol 22 (1) ◽  
pp. 55-63 ◽  
Author(s):  
SHIH-FANG FAN ◽  
STEPHEN YAZULLA
Keyword(s):  
G Protein ◽  
Receptor Agonist ◽  
Lucifer Yellow ◽  
Reciprocal Inhibition ◽  
Receptor Activation ◽  
Light Signal ◽  
Bipolar Cells ◽  
Protein G ◽  
Calcium Dependent ◽  
Voltage Dependent

Cannabinoid CB1receptor (viaGs) and dopamine D2receptor (viaGi/o) antagonistically modulate goldfish cone membrane currents. As ON bipolar cells have CB1and D1receptors, but not D2receptors, we focused on whether CB1receptor agonist and dopamine interact to modulate voltage-dependent outward membrane K+currentsIK(V)of the ON mixed rod/cone (Mb) bipolar cells. Whole-cell currents were recorded from Mb bipolar cells in goldfish retinal slices. Mb bipolar cells were identified by intracellular filling with Lucifer yellow. The bath solution was calcium-free and contained 1 mM cobalt to block indirect calcium-dependent effects. Dopamine (10 μM) consistently increasedIK(V)by a factor of 1.57 ± 0.12 (S.E.M.,n= 15). A CB receptor agonist, WIN 55212-2 (0.25–1 μM), had no effect, but 4 μM WIN 55212-2 suppressedIK(V)by 60%. IfIK(V)was first increased by 10 μM dopamine, application of WIN 55212-2 (0.25–1 μM) reversibly blocked the effect of dopamine even though these concentrations of WIN 55212-2 had no effect of their own. If WIN 55212-2 was applied first and dopamine (10 μM) was added to the WIN-containing solution, 0.1 μM WIN 55212-2 blocked the effect of dopamine. All effects of WIN 55212-2 were blocked by coapplication of SR 141716A (CB1antagonist) and pretreatment with pertussis toxin (blocker of Gi/o) indicating actionviaCB1receptor activation of G protein Gi/o. Coactivation of CB1and D1receptors on Mb bipolar cells produces reciprocal effects onIK(V). The CB1-evoked suppression ofIK(V)is mediated by G protein Gi/o, whereas the D1-evoked enhancement is mediated by G protein Gs. As dopamine is a retinal “light” signal, these data support our notion that endocannabinoids function as a “dark” signal, interacting with dopamine to set retinal sensitivity.

AGONIST ACTIVATED ADRENOCORTICOTROPIN RECEPTOR INTERNALIZES VIA A CLATHRIN-MEDIATED G PROTEIN RECEPTOR KINASE DEPENDENT MECHANISM

2002 ◽  
Vol 28 (4) ◽  
pp. 281-289 ◽  
Author(s):  
A. H. Baig ◽  
F. M. Swords ◽  
M. Szaszák ◽  
P. J. King ◽  
L. Hunyady ◽  
...  
Keyword(s):  
G Protein ◽  
Receptor Kinase ◽  
Protein Receptor ◽  
Dependent Mechanism

scholarly journals 199 Takotsubo syndrome associated mir-16 and mir-26a reduce contractility of cardiomyocytes in vitro by an inhibitory g-?protein dependent mechanism

Heart ◽  
2017 ◽  
Vol 103 (Suppl 5) ◽  
pp. A135.1-A135
Author(s):  
Liam Couch ◽  
Anselm A Derda ◽  
Thomas Thum ◽  
Cesare Terracciano ◽  
Sian Harding
Keyword(s):  
G Protein ◽  
Takotsubo Syndrome ◽  
Inhibitory G Protein ◽  
Dependent Mechanism
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