scholarly journals Reactive oxygen species alters the electrophysiological properties and raises [Ca2+]i in intracardiac ganglion neurons

2010 ◽  
Vol 299 (1) ◽  
pp. R42-R54 ◽  
Author(s):  
Jhansi Dyavanapalli ◽  
Katrina Rimmer ◽  
Alexander A. Harper
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Membrane Resistance ◽  
Resting Membrane Potential ◽  
Oxygen Species ◽  
Electrophysiological Properties ◽  
Control Value ◽  
Adult Rat ◽  
Ganglion Neurons ◽  
Ganglionic Transmission

We have investigated the effects of the reactive oxygen species (ROS) donors hydrogen peroxide (H2O2) and tert-butyl hydroperoxide ( t-BHP) on the intrinsic electrophysiological characteristics: ganglionic transmission and resting [Ca2+]i in neonate and adult rat intracardiac ganglion (ICG) neurons. Intracellular recordings were made using sharp microelectrodes filled with either 0.5 M KCl or Oregon Green 488 BAPTA-1, allowing recording of electrical properties and measurement of [Ca2+]i. H2O2 and t-BHP both hyperpolarized the resting membrane potential and reduced membrane resistance. In adult ICG neurons, the hyperpolarizing action of H2O2 was reversed fully by Ba2+ and partially by tetraethylammonium, muscarine, and linopirdine. H2O2 and t-BHP reduced the action potential afterhyperpolarization (AHP) amplitude but had no impact on either overshoot or AHP duration. ROS donors evoked an increase in discharge adaptation to long depolarizing current pulses. H2O2 blocked ganglionic transmission in most ICG neurons but did not alter nicotine-evoked depolarizations. By contrast, t-BHP had no significant action on ganglionic transmission. H2O2 and t-BHP increased resting intracellular Ca2+ levels to 1.6 ( ± 0.6, n = 11, P < 0.01) and 1.6 ( ± 0.3, n = 8, P < 0.001), respectively, of control value (1.0, ∼60 nM). The ROS scavenger catalase prevented the actions of H2O2, and this protection extended beyond the period of application. Superoxide dismutase partially shielded against the action of H2O2, but this was limited to the period of application. These data demonstrate that ROS decreases the excitability and ganglionic transmission of ICG neurons, attenuating parasympathetic control of the heart.

Abstract 1623: Reactive Oxygen Species increases Intracellular Calcium, alters the Electrophysiological Properties and Synaptic Transmission in Intrinsic Cardiac Ganglion Neurons: in vitro

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Jhansi Dyavanapalli ◽  
Katrina Rimmer ◽  
Alexander A Harper
Keyword(s):  
Reactive Oxygen Species ◽  
Synaptic Transmission ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Simultaneous Recording ◽  
Oxygen Species ◽  
Home Office ◽  
Electrophysiological Properties ◽  
Ganglion Neurons

Anerobic metabolism generates reactive oxygen species (ROS) as by-products and this is increased during ischemia. ROS have been shown to interact with and impair the functioning of membrane proteins such as ion channels and transporters and cause disturbances in intracellular Ca 2+ homeostasis. We have investigated the effects of ROS upon [Ca 2+ ] i , the intrinsic electrophysiological characteristics and synaptic transmission in neurons of the ICG regulating the sinoatrial node. The hypothesis is that ROS-induced damage increases [Ca 2+ ] i and attenuates synaptic transmission in ICG. used a whole-mount adult rat ICG preparation, in vitro (rats were killed by stunning and cervical dislocation, according to current UK Home Office guidelines). Intracellular recordings were made using sharp glass microelectrodes filled with Oregon Green 488 BAPTA-1, allowing simultaneous recording of electrical properties and measurement of [Ca 2+ ] i . Signals resulting from [Ca 2+ ] i changes were expressed as the ratio of fluorescence changes over baseline fluorescence, (f-fo)/fo . The ROS-donors hydrogen peroxide (H 2 O 2 , 1 mM) and tert-butyl hydroperoxide ( t -BHP, 1mM) had broadly similar actions on postganglionic somata, both producing membrane potential hyperpolarization (from −48.4 mV ± 6.5 S.D control to −69.9 mV ± 7.9 H 2 O 2 , n=7; and from −51.9 mV ± 7.1 control to −59.2 mV ± 7.9 t -BHP, n=17, p<0.001). Considering the somatic action potential (AP), t -BHP decreased the rate of rise (from 159 V/sec ± 79 control to 117 V/sec ± 53, n=6, p<0.05), but did not alter the rate of fall and increased AP duration (measured at 0 mV) from 0.7ms (± 0.2) control to 1.1ms (± 0.3, n=5, p<0.05). In addition, t -BHP reduced the AP afterhyper-polarization (AHP) amplitude (from 15.5 mV ± 5.2 control to 9.9 mV ± 4.5, n=10, p<0.001) but had no impact on AP overshoot or AHP duration. t -BHP and H 2 O 2 markedly increased resting [Ca 2+ ] i to 1.59 (± 0.03, n=8,p<0.001) and 2.36 (± 0.04, n=3, p<0.05) respectively, of control values (~ 60 nM ). H 2 O 2 blocked synaptic transmission in 3 /4 neurons. In contrast, t -BHP had no significant action on synaptic transmission. Together, these data demonstrate that ROS alters the excitability of ICG neurons attenuating parasympathetic control of the heart during ischemia/ reperfusion.

scholarly journals Aldosterone Stimulates Matrix Metalloproteinases and Reactive Oxygen Species in Adult Rat Ventricular Cardiomyocytes

Hypertension ◽  
2005 ◽  
Vol 46 (3) ◽  
pp. 555-561 ◽  
Author(s):  
Mary K. Rude ◽  
Toni-Ann S. Duhaney ◽  
Gabriela M. Kuster ◽  
Sharon Judge ◽  
Joline Heo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Matrix Metalloproteinases ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Adult Rat ◽  
Ventricular Cardiomyocytes

The Influence of Some Immunosuppressive Drugs on the Metabolic Activity of Human Phagocytes and Lymphocytes in vitro

1998 ◽  
Vol 11 (3) ◽  
pp. 155-162 ◽  
Author(s):  
M. Dušková ◽  
L. Dušek ◽  
M. Čìž ◽  
A. Lojek ◽  
H. Slavíková
Keyword(s):  
Reactive Oxygen Species ◽  
Cyclosporine A ◽  
Polymorphonuclear Leukocytes ◽  
Thymidine Incorporation ◽  
Reactive Oxygen ◽  
Blast Transformation ◽  
Oxygen Species ◽  
Fk 506 ◽  
Control Value

The effect of azathioprine, cyclosporine A and FK 506 on the production of reactive oxygen species by polymorphonuclear leukocytes (Iuminol-dependent chemiluminescence) and on the blast transformation of lymphocytes ([3H]thymidine incorporation) was studied in dose-response experiments under in vitro conditions. Although there were no significant effects of immunosuppressives on non-stimulated blast transformation, FK 506 and cyclosporine A significantly inhibited the blast transformation stimulated by concanavaline A and protein A and the effects made it possible to build 2nd-order polynomial dose-response models. Azathioprine was found to be a relatively weak inhibitor of [3H]thymidine incorporation in lymphocytes (76% of control value). Spontaneous production of reactive oxygen species by polymorphonuclear leukocytes was significantly inhibited, particularly by FK 506 (1–100 ng.ml−1) in comparison to the control value, while there was no effect of the immunosuppressives on this system activated either by starch grains or zymosan. Only the highest applied concentrations of azathioprine (100 ng.ml−1) and cyclosporine A (1000 ng.ml−1) led to a significant decline in spontaneous phagocytosis. The direct effect of immunosuppressives on activated production of reactive oxygen species by neutrophiles was not proved.

scholarly journals Combustion-derived flame generated ultrafine soot generates reactive oxygen species and activates Nrf2 antioxidants differently in neonatal and adult rat lungs

2013 ◽  
Vol 10 (1) ◽  
pp. 34 ◽  
Author(s):  
Jackie KW Chan ◽  
Jessica G Charrier ◽  
Sean D Kodani ◽  
Christoph F Vogel ◽  
Sarah Y Kado ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Adult Rat ◽  
Rat Lungs

fMLP-stimulated neutrophils increase endothelial [Ca2+]i and microvessel permeability in the absence of adhesion: role of reactive oxygen species

2005 ◽  
Vol 288 (3) ◽  
pp. H1331-H1338 ◽  
Author(s):  
Longkun Zhu ◽  
Vince Castranova ◽  
Pingnian He
Keyword(s):  
Reactive Oxygen Species ◽  
Leukocyte Adhesion ◽  
Reactive Oxygen ◽  
Iron Chelator ◽  
Oxygen Species ◽  
Control Value ◽  
Antioxidant Agents ◽  
Microvessel Permeability ◽  
Adhesion Role ◽  
Peak Value

Our previous study demonstrated that firm attachment of leukocytes to microvessel walls does not necessarily increase microvessel permeability ( Am J Physiol Heart Circ Physiol 283: H2420–H2430, 2002). To further understand the mechanisms of the permeability increase associated with leukocyte accumulation during acute inflammation, we investigated the direct relation of reactive oxygen species (ROS) release during neutrophil respiratory burst to changes in microvessel permeability and endothelial intracellular Ca2+ concentration ([Ca2+]i) in intact microvessels. ROS release from activated neutrophils was quantified by measuring changes in chemiluminescence. When isolated rat neutrophils (2 × 106/ml) were exposed to formyl-Met-Leu-Phe-OH (fMLP, 10 μM), chemiluminescence transiently increased from 1.2 ± 0.2 × 104 to a peak value of 6.7 ± 1.0 × 104 cpm/min ( n = 12). Correlatively, perfusing individual microvessels with fMLP-stimulated neutrophils in suspension (2 × 107/ml) increased hydraulic conductivity ( Lp) to 3.7 ± 0.4 times the control value ( n = 5) and increased endothelial [Ca2+]i from 84 ± 7 nM to a mean peak value of 170 ± 7 nM. In contrast, perfusing vessels with fMLP alone did not affect basal Lp. Application of antioxidant agents, superoxide dismutase, vitamin C, or an iron chelator, deferoxamine mesylate, attenuated ROS release in fMLP-stimulated neutrophils and abolished increases in Lp. These results indicate that release of ROS from fMLP-stimulated neutrophils increases microvessel permeability and endothelial [Ca2+]i independently from leukocyte adhesion and the migration process.

Role of reactive oxygen species and NAD(P)H oxidase in α1-adrenoceptor signaling in adult rat cardiac myocytes

2002 ◽  
Vol 282 (4) ◽  
pp. C926-C934 ◽  
Author(s):  
Lei Xiao ◽  
David R. Pimentel ◽  
Jing Wang ◽  
Krishna Singh ◽  
Wilson S. Colucci ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Ventricular Myocytes ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Extracellular Signal Regulated Kinase ◽  
Adult Rat ◽  
Transport Chain ◽  
Extracellular Signal ◽  
Hypertrophic Signaling ◽  
Oxide Synthase

We recently reported that α1-adrenoceptor (α1-AR) stimulation induces hypertrophy via activation of the mitogen/extracellular signal-regulated kinase (MEK) 1/2-extracellular signal-regulated kinase (ERK) 1/2 pathway and generates reactive oxygen species (ROS) in adult rat ventricular myocytes (ARVM). Here we investigate the intracellular source of ROS in ARVM and the mechanism by which ROS activate hypertrophic signaling after α1-AR stimulation. Pretreatment of ARVM with the ROS scavenger Mn(III)terakis(1-methyl-4-pyridyl) porphyrin pentachloride (MnTMPyP) completely inhibited the α1-AR-stimulated activation of Ras-MEK1/2-ERK1/2. Direct addition of H2O2or the superoxide generator menadione activated ERK1/2, which is also prevented by MnTMPyP pretreatment. We found that ARVM express gp91phox, p22phox, p67phox, and p47phox, four major components of NAD(P)H oxidase, and that α1-AR-stimulated ERK1/2 activation was blocked by four structurally unrelated inhibitors of NAD(P)H oxidase [diphenyleneiodonium, phenylarsine oxide, 4-(2-aminoethyl)benzenesulfonyl fluoride, and cadmium]. Conversely, inhibitors for other potential ROS-producing systems, including mitochondrial electron transport chain, nitric oxide synthase, xanthine oxidase, and cyclooxygenase, had no effect on α1-AR-stimulated ERK1/2 activation. Taken together, our results show that ventricular myocytes express components of an NAD(P)H oxidase that appear to be involved in α1-AR-stimulated hypertrophic signaling via ROS-mediated activation of Ras-MEK1/2-ERK1/2.

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