scholarly journals High Glucose Inhibits the Aspirin-Induced Activation of the Nitric Oxide/cGMP/cGMP-Dependent Protein Kinase Pathway and Does Not Affect the Aspirin-Induced Inhibition of Thromboxane Synthesis in Human Platelets

Diabetes ◽  
2012 ◽  
Vol 61 (11) ◽  
pp. 2913-2921 ◽  
Author(s):  
I. Russo ◽  
M. Viretto ◽  
C. Barale ◽  
L. Mattiello ◽  
G. Doronzo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
High Glucose ◽  
Human Platelets ◽  
Dependent Protein Kinase ◽  
Cgmp Dependent Protein Kinase ◽  
Dependent Protein ◽  
Kinase Pathway

scholarly journals Heat Shock Protein 27 Is a Substrate of cGMP-dependent Protein Kinase in Intact Human Platelets

2000 ◽  
Vol 276 (10) ◽  
pp. 7108-7113 ◽  
Author(s):  
Elke Butt ◽  
Dorian Immler ◽  
Helmut E. Meyer ◽  
Alexey Kotlyarov ◽  
Kathrin Laaß ◽  
...  
Keyword(s):  
Heat Shock ◽  
Protein Kinase ◽  
Heat Shock Protein ◽  
Heat Shock Protein 27 ◽  
Human Platelets ◽  
Dependent Protein Kinase ◽  
Cgmp Dependent Protein Kinase ◽  
Dependent Protein

scholarly journals TREK-1 Regulation by Nitric Oxide and cGMP-dependent Protein Kinase

2001 ◽  
Vol 276 (47) ◽  
pp. 44338-44346 ◽  
Author(s):  
Sang Don Koh ◽  
Kevin Monaghan ◽  
Gerard P. Sergeant ◽  
Seungil Ro ◽  
Rebecca L. Walker ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Dependent Protein Kinase ◽  
Cgmp Dependent Protein Kinase ◽  
Dependent Protein

scholarly journals Testosterone-induced relaxation of coronary arteries: activation of BKCa channels via the cGMP-dependent protein kinase

2012 ◽  
Vol 302 (1) ◽  
pp. H115-H123 ◽  
Author(s):  
Viju Deenadayalu ◽  
Yashoda Puttabyatappa ◽  
Alexander T. Liu ◽  
John N. Stallone ◽  
Richard E. White
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Protein Kinase ◽  
Coronary Arteries ◽  
Specific Inhibitor ◽  
No Production ◽  
Channel Activity ◽  
Dependent Protein Kinase ◽  
Cgmp Dependent Protein Kinase ◽  
Dependent Protein

Androgens are reported to have both beneficial and detrimental effects on human cardiovascular health. The aim of this study was to characterize nongenomic signaling mechanisms in coronary artery smooth muscle (CASM) and define the ionic basis of testosterone (TES) action. TES-induced relaxation of endothelium-denuded porcine coronary arteries was nearly abolished by 20 nM iberiotoxin, a highly specific inhibitor of large-conductance, calcium-activated potassium (BKCa) channels. Molecular patch-clamp studies confirmed that nanomolar concentrations of TES stimulated BKCa channel activity by ∼100-fold and that inhibition of nitric oxide synthase (NOS) activity by NG-monomethyl-l-arginine nearly abolished this effect. Inhibition of nitric oxide (NO) synthesis or guanylyl cyclase activity also attenuated TES-induced coronary artery relaxation but did not alter relaxation due to 8-bromo-cGMP. Furthermore, we detected TES-stimulated NO production in porcine coronary arteries and in human CASM cells via stimulation of the type 1 neuronal NOS isoform. Inhibition of the cGMP-dependent protein kinase (PKG) attenuated TES-stimulated BKCa channel activity, and direct assay determined that TES increased activity of PKG in a concentration-dependent fashion. Last, the stimulatory effect of TES on BKCa channel activity was mimicked by addition of purified PKG to the cytoplasmic surface of a cell-free membrane patch from CASM myocytes (∼100-fold increase). These findings indicate that TES-induced relaxation of endothelium-denuded coronary arteries is mediated, at least in part, by enhanced NO production, leading to cGMP synthesis and PKG activation, which, in turn, opens BKCa channels. These findings provide a molecular mechanism that could help explain why androgens have been reported to relax coronary arteries and relieve angina pectoris.

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