Interaction between nitric oxide signaling and gap junctions during ischemic preconditioning: Importance of S-nitrosylation vs. protein kinase G activation

Nitric Oxide ◽  
2017 ◽  
Vol 65 ◽  
pp. 37-42 ◽  
Author(s):  
Fei Xie ◽  
Bing Rong ◽  
Tian-cheng Wang ◽  
Li Hao ◽  
Ming-jie Lin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Gap Junctions ◽  
Ischemic Preconditioning ◽  
Protein Kinase G ◽  
Nitric Oxide Signaling

Nitric oxide signaling inhibits microglia proliferation by activation of protein kinase-G

Nitric Oxide ◽  
2020 ◽  
Vol 94 ◽  
pp. 125-134 ◽  
Author(s):  
Matthew J.E. Maksoud ◽  
Vasiliki Tellios ◽  
Yun-Yan Xiang ◽  
Wei-Yang Lu
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Protein Kinase G ◽  
Nitric Oxide Signaling

Interplay of VIP and nitric oxide in regulation of the descending relaxation phase of peristalsis

1993 ◽  
Vol 264 (2) ◽  
pp. G334-G340 ◽  
Author(s):  
J. R. Grider
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Protein Kinase ◽  
Protein Kinase G ◽  
Rat Colon ◽  
No Production ◽  
Field Stimulation ◽  
Relaxant Effect ◽  
Relaxation Phase ◽  
Kinase A

Involvement of vasoactive intestinal peptide (VIP) and nitric oxide (NO) in neurally induced relaxation was examined in smooth muscle from rat colon. Relaxation induced by field stimulation or radial stretch (i.e., descending relaxation phase of the peristaltic reflex) was accompanied by VIP release and NO production. NG-nitro-L-arginine (L-NNA) abolished NO production in both preparations but only partly inhibited VIP release (45 +/- 8% at 8 Hz and 59 +/- 10% at 10 g stretch) and relaxation (62 +/- 5% and 35 +/- 6%); the effect of L-NNA was reversed by L-arginine but not D-arginine. The pattern implied that NO production normally acts to enhance VIP release. In addition, VIP induced relaxation and stimulated NO production in muscle strips and isolated colonic muscle cells: L-NNA abolished NO production but only partly inhibited relaxation (58 +/- 6%); oxyhemoglobin had no effect. The effect of L-NNA on relaxation was reversed by L-arginine but not by D-arginine. The protein kinase A inhibitor (R)-p-adenosine 3',5'-cyclic phosphorothioate [(R)-p-cAMPS] and the protein kinase G inhibitor KT5823 inhibited VIP-induced relaxation by 76 +/- 5 and 35 +/- 4%, respectively; a combination of the two inhibitors abolished relaxation. (R)-p-cAMPS blocked the direct relaxant effect of VIP, whereas KT5823 blocked the indirect effect of VIP mediated by NO.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals cGMP/Protein Kinase G-Dependent Inhibition of N-Type Ca2+Channels Induced by Nitric Oxide in Human Neuroblastoma IMR32 Cells

2002 ◽  
Vol 22 (17) ◽  
pp. 7485-7492 ◽  
Author(s):  
Marcello D'Ascenzo ◽  
Giovanni Martinotti ◽  
Gian Battista Azzena ◽  
Claudio Grassi
Keyword(s):  
Nitric Oxide ◽  
Protein Kinase ◽  
Protein Kinase G ◽  
Human Neuroblastoma ◽  
Dependent Inhibition ◽  
Ca2 Channels
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