Relaxing effect of a new ruthenium complex nitric oxide donor on airway smooth muscle of an experimental model of asthma in rats

2016 ◽  
Vol 43 (2) ◽  
pp. 221-229 ◽  
Author(s):  
Patrícia Ferreira da Silva Castro ◽  
Daniela Lobo de Andrade ◽  
Carolina de Fátima Reis ◽  
Sérgio Henrique Nascente Costa ◽  
Aline Carvalho Batista ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Experimental Model ◽  
Airway Smooth Muscle ◽  
Ruthenium Complex ◽  
Nitric Oxide Donor ◽  
Relaxing Effect

A new nitrosyl ruthenium complex nitric oxide donor presents higher efficacy than sodium nitroprusside on relaxation of airway smooth muscle

2011 ◽  
Vol 43 (5) ◽  
pp. 370-377 ◽  
Author(s):  
Patrícia F.S. Castro ◽  
Amanda de C. Pereira ◽  
Gerson J. Rogrigues ◽  
Aline C. Batista ◽  
Roberto S. da Silva ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Sodium Nitroprusside ◽  
Airway Smooth Muscle ◽  
Ruthenium Complex ◽  
Nitric Oxide Donor

scholarly journals Cyclic nucleotide regulation of store-operated Ca2+ influx in airway smooth muscle

2006 ◽  
Vol 290 (2) ◽  
pp. L278-L283 ◽  
Author(s):  
Binnaz Ay ◽  
Adeyemi Iyanoye ◽  
Gary C. Sieck ◽  
Y. S. Prakash ◽  
Christina M. Pabelick
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Protein Kinase ◽  
Protein Kinases ◽  
Airway Smooth Muscle ◽  
Cyclic Nucleotides ◽  
Cyclopiazonic Acid ◽  
Nitric Oxide Donor ◽  
Cgmp Analog ◽  
Intracellular Ca

Sarcoplasmic reticulum (SR) Ca2+ release and plasma membrane Ca2+ influx are key to intracellular Ca2+ ([Ca2+]i) regulation in airway smooth muscle (ASM). SR Ca2+ depletion triggers influx via store-operated Ca2+ channels (SOCC) for SR replenishment. Several clinically relevant bronchodilators mediate their effect via cyclic nucleotides (cAMP, cGMP). We examined the effect of cyclic nucleotides on SOCC-mediated Ca2+ influx in enzymatically dissociated porcine ASM cells. SR Ca2+ was depleted by 1 μM cyclopiazonic acid in 0 extracellular Ca2+ ([Ca2+]o), nifedipine, and KCl (preventing Ca2+ influx through L-type and SOCC channels). SOCC was then activated by reintroduction of [Ca2+]o and characterized by several techniques. We examined cAMP effects on SOCC by activating SOCC in the presence of 1 μM isoproterenol or 100 μM dibutryl cAMP (cell-permeant cAMP analog), whereas we examined cGMP effects using 1 μM (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO nitric oxide donor) or 100 μM 8-bromoguanosine 3',5'-cyclic monophosphate (cell-permeant cGMP analog). The role of protein kinases A and G was examined by preexposure to 100 nM KT-5720 and 500 nM KT-5823, respectively. SOCC-mediated Ca2+ influx was dependent on the extent of SR Ca2+ depletion, sensitive to Ni2+ and La3+, but not inhibitors of voltage-gated influx channels. cAMP as well as cGMP potently inhibited Ca2+ influx, predominantly via their respective protein kinases. Additionally, cAMP cross-activation of protein kinase G contributed to SOCC inhibition. These data demonstrate that a Ni2+/La3+-sensitive Ca2+ influx in ASM triggered by SR Ca2+ depletion is inhibited by cAMP and cGMP via a protein kinase mechanism. Such inhibition may play a role in the bronchodilatory response of ASM to clinically relevant drugs (e.g., β-agonists vs. nitric oxide).

Silver nanoparticles Induce Anti-Proliferative Effects on Airway Smooth Muscle Cells. Role of Nitric Oxide and Muscarinic Receptor Signaling Pathway

2013 ◽  
Vol 65 ◽  
pp. S104
Author(s):  
Manuel Alejandro Ramirez-Lee ◽  
Hector Rosas-Hernandez ◽  
Samuel Salazar-Garcia ◽  
Jose Manuel Gutiérrez-Hernández ◽  
Ricardo Espinosa- Tanguma ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Silver Nanoparticles ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Signaling Pathway ◽  
Muscarinic Receptor ◽  
Airway Smooth Muscle ◽  
Airway Smooth Muscle Cells ◽  
Receptor Signaling Pathway

HPLC separation, NMR and QTOF/MS/MS structure elucidation of a prominent nitric oxide donor agent based on an isomeric composition of a nitrosyl ruthenium complex

2009 ◽  
Vol 12 (5) ◽  
pp. 343-346 ◽  
Author(s):  
Anderson Rodrigo Moraes de Oliveira ◽  
Franciane Marquele-Oliveira ◽  
Danielle Cristine Almeida Silva de Santana ◽  
Sofia Nikolaou ◽  
Pierina Sueli Bonato ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Structure Elucidation ◽  
Ruthenium Complex ◽  
Nitric Oxide Donor ◽  
Isomeric Composition ◽  
Hplc Separation ◽  
Agent Based

Adenosine receptor-mediated relaxation of rabbit airway smooth muscle: a role for nitric oxide

1997 ◽  
Vol 273 (3) ◽  
pp. L581-L587 ◽  
Author(s):  
S. Ali ◽  
W. J. Metzger ◽  
H. A. Olanrewaju ◽  
S. J. Mustafa
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Epithelial Cells ◽  
Airway Smooth Muscle ◽  
Adenosine Receptor ◽  
Inhibitory Effect ◽  
No Production ◽  
Relaxant Effect ◽  
Adenosine Receptor Agonists ◽  
Cgs 21680

In this study, we investigated the relaxant effect of adenosine receptor agonists on KCl-precontracted airway smooth muscle from rabbits and characterized the type of receptor involved in bronchorelaxation in the presence and absence of epithelium. We further defined the role of epithelium-derived relaxing factor, i.e., nitric oxide (NO), on these responses. In both epithelium-intact and -denuded tertiary airway rings from rabbits, the adenosine receptor agonists 2-[p-(2-carboxyethyl)]phenylethylamino-5-N'-ethylcarboxamidoadenos ine (CGS-21680), 5'-(N-ethyl-carboxamido)adenosine (NECA), 2-chloroadenosine (CAD), and (-)-N6-(2-phenylisopropyl)adenosine (R-PIA) relaxed airway smooth muscle with a potency order of CGS-21680 > NECA > CAD > R-PIA. A 98.5, 89.7, 73.2, and 64.7% relaxation was observed at 10(-5) M by CGS-21680, NECA, CAD, and R-PIA in the epithelium-intact bronchial rings, respectively. The 50% maximum effective concentration (EC50; x 10(-7) M) values for CGS-21680, NECA, CAD, and R-PIA were 2, 4, 9, and 80, respectively. Denuded rings, however, showed much less relaxant responses to various adenosine agonists compared with epithelium-intact rings. The adenosine receptor antagonist 8-(sulfophenyl)theophylline significantly attenuated the relaxant responses to all the agonists in the epithelium-intact and -denuded rings. The epithelium-dependent relaxant effect of the agonists in airway rings was inhibited by NG-monomethyl-L-arginine (L-NMMA; 30 microM). The EC50 (x 10(-6) M) values for CGS-21680, NECA, CAD, and R-PIA in the presence of inhibitor were 5.5, 8, 30, and 200, respectively. The L-NMMA produced an insignificant inhibitory effect in the epithelium-denuded rings. L-Arginine but not D-arginine (100 microM) reversed the inhibitory effect of L-NMMA on adenosine agonist-induced relaxation. In primary epithelial cells in culture, CGS-21680 (10(-5) M) induced a fourfold increase in NO production over the control. The CGS-21680-induced NO production in epithelial cells was significantly inhibited by NG-nitro-L-arginine methyl ester (L-NAME). Moreover, L-arginine reversed the inhibitory effect of L-NAME in the epithelial cells. The data suggest that adenosine relaxes rabbit airway smooth muscle through an A2 adenosine receptor and the epithelium serves as a source of NO.

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