Asenapine modulates nitric oxide release and calcium movements in cardyomyoblasts

2016 ◽  
Vol 33 (S1) ◽  
pp. S553-S553
Author(s):  
P. Zeppegno ◽  
C. Gramaglia ◽  
E. Gattoni ◽  
S. Gili ◽  
E. Gambaro ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Clinical Relevance ◽  
Nitric Oxide Release ◽  
No Release ◽  
Intracellular Ca ◽  
Specific Receptors ◽  
Competing Interest ◽  
Dopaminergic Antagonists ◽  
Serotoninergic Receptors

ObjectiveTo examine the effects of asenapine on NO release and Ca2+ transients in H9C2, which were either subjected to peroxidation or not.Materials and methodsH9C2 were treated with asenapine alone or in presence of intracellular kinases blockers, serotoninergic and dopaminergic antagonists, and voltage Ca2+ channels inhibitors. Experiments were also performed in H9C2 treated with hydrogen peroxide. NO release and intracellular Ca2+ were measured through specific probes.ResultsIn H9C2, asenapine differently modulated NO release and Ca2+ movements depending on the peroxidative condition. The Ca2+ pool mobilized by asenapine mainly originated from the extracellular space and was slightly affected by thapsigargin. Moreover, the effects of asenapine were reduced or prevented by kinases blockers, dopaminergic and serotoninergic receptors inhibitors and voltage Ca2+ channels blockers.ConclusionsOn the basis of our findings we can conclude that asenapine by interacting with its specific receptors, exerts dual effects on NO release and Ca2+ homeostasis in H9C2; this would be of particular clinical relevance, when considering their role in cardiac function modulation.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Retracted Article: Light-triggered nitric oxide release and targeted fluorescence imaging in tumor cells developed from folic acid-graft-carboxymethyl chitosan nanospheres

RSC Advances ◽  
2014 ◽  
Vol 4 (57) ◽  
pp. 30129-30136 ◽  
Author(s):  
Rijun Gui ◽  
Ajun Wan ◽  
Yalei Zhang ◽  
Huili Li ◽  
Tingting Zhao
Keyword(s):  
Nitric Oxide ◽  
Folic Acid ◽  
Tumor Cells ◽  
Fluorescence Imaging ◽  
Carboxymethyl Chitosan ◽  
Nitric Oxide Release ◽  
No Release ◽  
Retracted Article ◽  
Potential Applications

This article reported the synthesis of CMC–FA–RBS(CQD) nanospheres and studied their potential applications for NO release and fluorescence imaging.

scholarly journals Nitric oxide release by N-(2-chloroethyl)-N-nitrosoureas: a rarely discussed mechanistic path towards their anticancer activity

RSC Advances ◽  
2015 ◽  
Vol 5 (3) ◽  
pp. 2137-2146
Author(s):  
Amrita Sarkar ◽  
Subhendu Karmakar ◽  
Sudipta Bhattacharyya ◽  
Kallol Purkait ◽  
Arindam Mukherjee
Keyword(s):  
Nitric Oxide ◽  
Anticancer Activity ◽  
Nitric Oxide Release ◽  
No Release

Our work shows that NO release is a feasible pathway of action for aromatic and heterocyclic N-(2-chloroethyl)-N-nitrosoureas and faster NO release may not lead to higher cytotoxicity.

Direct measurement of nitric oxide release from vascular endothelial cells

1996 ◽  
Vol 81 (2) ◽  
pp. 774-779 ◽  
Author(s):  
J. P. Guo ◽  
T. Murohara ◽  
M. Buerke ◽  
R. Scalia ◽  
A. M. Lefer
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Methyl Ester ◽  
Vascular Endothelial Cells ◽  
Calmodulin Antagonist ◽  
Nitric Oxide Release ◽  
A 23187 ◽  
No Release ◽  
Basal Release ◽  
Isolated Rat

A nitric oxide (NO)-selective electrode was used to directly measure NO release from isolated rat aortic endothelium and cultured rat aortic endothelial cells (RAECs). Basal release of NO was significantly attenuated by a NO synthase inhibitor NG-nitro-L-arginine methyl ester (1 mM) to 42 +/- 14 pmol/1 x 10(5) cells (P < 0.01). The basal release of NO was also significantly inhibited by a calmodulin antagonist W-7 at 15 microM (P < 0.01). L-Arginine (1 mM), significantly stimulated NO release (P < 0.05 vs. control basal release). Stimulation of cultured RAECs with two endothelium-dependent vasodilators, acetylcholine (100 nM) and A-23187 (1 microM), significantly increased NO release [574 +/- 112 pmol/1 x 10(5) cells (n = 5) and 658 +/- 119 pmol/1 x 10(5) cells (n = 5) in acetylcholine- and A-23187-stimulated RAECs, respectively]. Basal release of NO was also detectable in isolated rat aortic rings with intact endothelium. NO release was significantly attenuated by NG-nitro-L-arginine methyl ester and augmented by human superoxide dismutase. These data indicate the physiological usefulness of the amperometric measurement of NO employing a NO-specific electrode in biological systems.

scholarly journals Functionalized graphene-based biomimetic microsensor interfacing with living cells to sensitively monitor nitric oxide release

2015 ◽  
Vol 6 (3) ◽  
pp. 1853-1858 ◽  
Author(s):  
Yan-Ling Liu ◽  
Xue-Ying Wang ◽  
Jia-Quan Xu ◽  
Chong Xiao ◽  
Yan-Hong Liu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Real Time ◽  
Living Cells ◽  
Functionalized Graphene ◽  
Nitric Oxide Release ◽  
No Release

We present a biomimetic and reusable microsensor with sub-nanomolar sensitivity by elaboratly functionalizing graphene for monitoring NO release in real-time.

Reduced perivascular Po2 increases nitric oxide release from endothelial cells

2003 ◽  
Vol 285 (2) ◽  
pp. H507-H515 ◽  
Author(s):  
G. P. Nase ◽  
J. Tuttle ◽  
H. G. Bohlen
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Parenchymal Cell ◽  
Oxygen Availability ◽  
No Production ◽  
Main Site ◽  
Nitric Oxide Release ◽  
No Release ◽  
Parenchymal Cells

Many studies have suggested that endothelial cells can act as “oxygen sensors” to large reductions in oxygen availability by increasing nitric oxide (NO) production. This study determined whether small reductions in oxygen availability enhanced NO production from in vivo intestinal arterioles, venules, and parenchymal cells. In vivo measurements of perivascular NO concentration ([NO]) were made with NO-sensitive microelectrodes during normoxic and reduced oxygen availability. During normoxia, intestinal first-order arteriolar [NO] was 397 ± 26 nM ( n = 5), paired venular [NO] was 298 ± 34 nM ( n = 5), and parenchymal cell [NO] was 138 ± 36 nM ( n = 3). During reduced oxygen availability, arteriolar and venular [NO] significantly increased to 695 ± 79 nM ( n = 5) and 534 ± 66 nM ( n = 5), respectively, whereas parenchymal [NO] remained unchanged at 144 ± 34 nM ( n = 4). During reduced oxygenation, arteriolar and venular diameters increased by 15 ± 3% and 14 ± 5%, respectively: NG-nitro-l-arginine methyl ester strongly suppressed the dilation to lower periarteriolar Po2. Micropipette injection of a CO2 embolus into arterioles significantly attenuated arteriolar dilation and suppressed NO release in response to reduced oxygen availability. These results indicated that in rat intestine, reduced oxygen availability increased both arteriolar and venular NO and that the main site of NO release under these conditions was from endothelial cells.

SB-220453, A Potential Novel Antimigraine Agent, Inhibits Nitric Oxide Release Following Induction of Cortical Spreading Depression in the Anaesthetized Cat

Cephalalgia ◽  
2000 ◽  
Vol 20 (2) ◽  
pp. 92-99 ◽  
Author(s):  
SJ Read ◽  
MI Smith ◽  
AJ Hunter ◽  
N Upton ◽  
AA Parsons
Keyword(s):  
Nitric Oxide ◽  
Median Duration ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Therapeutic Potential ◽  
Field Potential ◽  
Current Field ◽  
Nitric Oxide Release ◽  
Haemodynamic Parameters ◽  
No Release

Profound nitric oxide release associated with cortical spreading depression (SD), has been implicated in stroke, traumatic brain injury and migraine pathophysiology. SB-220453 represents a mechanistically novel, well-tolerated class of compounds which may have therapeutic potential in the treatment of conditions associated with neuronal hyperexcitability and inflammation. The aim of the present study was to investigate the effects of SB-220453 on the nitric oxide (NO) release associated with SD in the anaesthetized cat. In vehicle treated animals, KCl application for 6 min to the cortical suface produced repeated changes in extracellular direct current field potential with associated NO release. This activity was sustained for a median duration of 55 min (25–75% range, 32–59 min) and 59 min (25–75% range, 34–59 min), respectively. SB-220453 (1, 3 and 10 mg/kg i.p.) produced a dose-related inhibition of this activity and at the highest dose tested, the median duration of changes in extracellular field potential and NO release were reduced to 4 min (25–75% range, 4–5min) and 5 min (25–75% range, 5–5min), respectively. No effect was observed on basal systemic haemodynamic parameters or resting cerebral laser Doppler blood flux at any of the doses of SB-220453 tested. SB-220453 therefore represents a novel compound to assess the potential benefit of inhibiting SD associated nitric oxide release in neurological disease.

Peritubular fluid viscosity modulates H+ flux in proximal tubules through NO release

2001 ◽  
Vol 280 (2) ◽  
pp. F239-F243 ◽  
Author(s):  
Paula Díaz-Sylvester ◽  
Myriam Mac Laughlin ◽  
Carlos Amorena
Keyword(s):  
Nitric Oxide ◽  
Inhibitory Effect ◽  
Proximal Tubules ◽  
Fluid Viscosity ◽  
Peritubular Capillary ◽  
Reactive Blue 2 ◽  
Nitric Oxide Release ◽  
Control Value ◽  
Peritubular Capillaries ◽  
No Release

We evaluated the effects of increasing the viscosity (η) in peritubular capillary perfusates (PCP; 20 mM HNaPO4 −-Ringer, pH 7.4) on proximal convoluted tubule (PCT) acidification. Micropuncture experiments were performed with simultaneous luminal and peritubular perfusion. Changes in pH of a 20 mM HNaPO4 −-Ringer (pH 7.4 at t = 0) droplet placed in PCT lumen were measured with H+-sensitive microelectrodes. By adding neutral dextran (molecular wt 300,000–400,000) to the PCP, η was increased. The effect of 10−5 M ATP added to normal-η PCP was evaluated. High η increased H+ flux (85 and 97% when η was increased 20 and 30%, respectively, above the control value). This increase was abolished by adding the nitric oxide antagonist N ω-nitro-l-arginine (l-NNA; 10−4 M) or the purinoreceptor antagonists suramin (10−4 M) and reactive blue 2 (3 × 10−5 M). Addition of 5 × 10−3 Ml-arginine to the peritubular perfusate overcame the inhibitory effect of l-NNA on high-η-induced increase in H+ flux. ATP increased H+ flux (80%), and this effect was blocked by l-NNA. These results suggest that changes in η can modulate proximal H+ flux, at least in part, through ATP-dependent nitric oxide release from the endothelial cells of the peritubular capillaries.

scholarly journals 20-HETE-induced nitric oxide production in pulmonary artery endothelial cells is mediated by NADPH oxidase, H2O2, and PI3-kinase/Akt

2010 ◽  
Vol 298 (4) ◽  
pp. L564-L574 ◽  
Author(s):  
Sreedhar Bodiga ◽  
Stephanie K. Gruenloh ◽  
Ying Gao ◽  
Vijay L. Manthati ◽  
Narsimhaswamy Dubasi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Nadph Oxidase ◽  
Pi3 Kinase ◽  
No Production ◽  
Akt Inhibitor ◽  
Akt Phosphorylation ◽  
No Release

We have shown that 20-hydroxyeicosatetraenoic acid (20-HETE) increases both superoxide and nitric oxide (NO) production in bovine pulmonary artery endothelial cells (BPAECs). The current study was designed to determine mechanisms underlying 20-HETE-stimulated NO release, and particularly the role of NADPH oxidase, reactive oxygen species, and PI3-kinase in stimulated NO release. Intracellular hydrogen peroxide (H2O2) and NO production were detected by dichlorofluorescein or dihydrorhodamine and diaminofluorescein fluorescence, respectively. Activation of endothelial nitric oxide synthase (eNOS) (Ser1179) and Akt (Ser473) was assessed by comparing the ratio of phosphorylated to total protein expression by Western blotting. Addition of 20-HETE to BPAECs caused an increase in superoxide and hydrogen peroxide, but not peroxynitrite. 20-HETE-evoked activation of Akt and eNOS, as well as enhanced NO release, are dependent on H2O2 as opposed to superoxide in that these endpoints are blocked by PEG-catalase and not PEG-superoxide dismutase. Similarly, 20-HETE-stimulated NO production in BPAECs is blocked by NADPH oxidase inhibitors apocynin or gp91 blocking peptide, and by PI3-kinase/Akt blockers wortmannin, LY-294002, or Akt inhibitor, implicating NADPH oxidase, PI3-kinase, and Akt signaling pathways, respectively, in this process. Together, these data suggest the following scheme: 20-HETE stimulates NADPH oxidase-dependent formation of superoxide. Superoxide is rapidly dismutated to hydrogen peroxide, which then mediates activation of PI3-kinase/Akt, phosphorylation of eNOS, and enhanced release of NO from eNOS in response to 20-HETE in BPAECs.

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