Homocysteine-induced changes in vascular reactivity of guinea-pig pulmonary arteries: Role of the oxidative stress and poly (ADP-ribose) polymerase activation

2007 ◽  
Vol 20 (3) ◽  
pp. 265-272 ◽  
Author(s):  
Arda Tasatargil ◽  
Gulay Sadan ◽  
Edibe Karasu
Keyword(s):  
Oxidative Stress ◽  
Guinea Pig ◽  
Vascular Reactivity ◽  
Pulmonary Arteries ◽  
Induced Changes

Role of Oxidative Stress in Ischemia–Reperfusion-Induced Changes in Na+,K+-ATPase Isoform Expression in Rat Heart

2004 ◽  
Vol 6 (5) ◽  
pp. 914-923 ◽  
Author(s):  
Petr Ostadal ◽  
Adel B. Elmoselhi ◽  
Irena Zdobnicka ◽  
Anton Lukas ◽  
Vijayan Elimban ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isoform Expression ◽  
Induced Changes

Role of Oxidative Stress in Ischemia–Reperfusion-Induced Changes in Na+,K+-ATPase Isoform Expression in Rat Heart

2004 ◽  
Vol 6 (5) ◽  
pp. 914-923 ◽  
Author(s):  
Petr Ostadal ◽  
Adel B. Elmoselhi ◽  
Irena Zdobnicka ◽  
Anton Lukas ◽  
Vijayan Elimban ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Heart ◽  
Ischemia Reperfusion ◽  
Isoform Expression ◽  
Induced Changes

Role of Oxidative Stress in Catecholamine-Induced Changes in Cardiac Sarcolemmal Ca2+ Transport

2001 ◽  
Vol 387 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Paramjit S. Tappia ◽  
Tomoji Hata ◽  
Lena Hozaima ◽  
Manjot S. Sandhu ◽  
Vincenzo Panagia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Induced Changes

Role of Neuroimaging Modality in the Assessment of Oxidative Stress in Brain: A Comprehensive Review

2019 ◽  
Vol 18 (5) ◽  
pp. 372-381 ◽  
Author(s):  
Vikas Pareek ◽  
Banshi Nath ◽  
Prasun K. Roy
Keyword(s):  
Oxidative Stress ◽  
Diffusion Tensor ◽  
Apoptotic Cell ◽  
Review Article ◽  
Present Review ◽  
Resonance Spectroscopy ◽  
Secondary Source ◽  
Longitudinal Assessment ◽  
Induced Changes

Background & Objective:Oxidative stress (OS) is the secondary source of an injury in consequence to the earlier caused primary injury; it is the condition of an imbalance between oxidants and antioxidants within the physiological system. OS causes alterations in proteins and DNA structure, leading to inflammation, apoptotic cell death, and tissue damage. Neurodegenerative diseases (NDDs) such as Alzheimer's disease, Parkinson's disease, Glioma-induced neurodegeneration and the normal aging-related neuro-degeneration are primarily associated with the increased OS. The present review article is committed to delivering a comprehensive overview of the current neuroimaging modalities which estimates an indirect correlate of OS in the brain. OS-induced changes in white matter tracts and the gray matter volumes are reviewed assessing the role of diffusion tensor imaging (DTI) and voxel-based morphometry (VBM) respectively. Further, the role of magnetic resonance spectroscopy (MRS) to assess the OS-induced alterations of chemical moieties, and thus the resultant structural implications in the neurological disorders are also briefly as well as precisely reviewed.Conclusions:In the present review article we present an overview of the role of neuroimaging modalities in the diagnosis, and longitudinal assessment during treatment of the OS induced changes.

Endogenous vasodilators modulate pulmonary vascular anaphylaxis

1994 ◽  
Vol 76 (2) ◽  
pp. 916-922 ◽  
Author(s):  
L. J. Kelly ◽  
B. J. Undem ◽  
G. K. Adams
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Methyl Ester ◽  
Guinea Pig ◽  
Initial Phase ◽  
Contractile Response ◽  
Pulmonary Arteries ◽  
Relaxing Factor ◽  
Anaphylactic Contraction

We examined the role of endothelium-derived nitric oxide during antigen-induced contraction in pulmonary arteries isolated from actively sensitized guinea pigs. Ovalbumin (10(-2) mg/ml)-induced contraction was not sustained, and tension returned to baseline within 15 min. Pretreatment with methylene blue (10(-5) M) increased both the amplitude and the duration of the contractile response in these tissues. At 15 min, tension remained elevated and was > 70% of the peak amplitude. Removal of the endothelium with saponin (200 micrograms/ml) increased the magnitude of the contraction by > 125%; however, the duration of the response was unaffected. After pretreatment with saponin, methylene blue no longer increased the amplitude of antigen-induced contraction but its effect on the duration was unchanged. Pretreatment with nitro-L-arginine methyl ester significantly increased the magnitude of the contraction in each of the tissues. These results suggest that the response of guinea pig pulmonary arteries to antigen is modulated by two types of endogenous vasodilators, endothelium-derived nitric oxide that inhibits the initial phase of the response and an endothelium-independent relaxing factor that is guanosine 3′,5′-cyclic monophosphate dependent and attenuates the duration of anaphylactic contraction.

Intracellular acidosis differentially regulates KV channels in coronary and pulmonary vascular muscle

1998 ◽  
Vol 275 (4) ◽  
pp. H1351-H1359 ◽  
Author(s):  
Marcie G. Berger ◽  
Christophe Vandier ◽  
Pierre Bonnet ◽  
William F. Jackson ◽  
Nancy J. Rusch
Keyword(s):  
Vascular Reactivity ◽  
Pulmonary Arteries ◽  
Cell Types ◽  
Resistance Arteries ◽  
Intracellular Acidosis ◽  
Pipette Solution ◽  
Voltage Gated ◽  
Kv Channels ◽  
Ionic Mechanisms ◽  
Induced Changes

Decreases in intracellular pH (pHi) potently dilate coronary resistance arteries but constrict small pulmonary arteries. To define the ionic mechanisms of these responses, this study investigated whether acute decreases in pHi differentially regulate K+ currents in single vascular smooth muscle (VSM) cells isolated from rat coronary and pulmonary resistance arteries. In patch-clamp studies, whole cell K+ currents were elicited by 10-mV depolarizing steps between −60 and 0 mV in VSM cells obtained from 50- to 150-μm-OD arterial branches, and pHi was lowered by altering the NH4Cl gradient across the cell membrane. Progressively lowering pHi from calculated values of 7.0 to 6.7 and 6.4 increased the peak amplitude of K+ current in coronary VSM cells by 15 ± 5 and 23 ± 3% but reduced K+ current in pulmonary VSM cells by 18 ± 3 and 21 ± 3%, respectively. These changes were reversed by returning cells to the control pHi of 7.0 and were eliminated by dialyzing cells with pipette solution containing 50 mmol/l HEPES to buffer NH4Cl-induced changes in pHi. Pharmacological block of ATP-sensitive K+ channels and Ca2+-activated K+ channels by 1 μmol/l glibenclamide and 100 nmol/l iberiotoxin, respectively, did not prevent changes in K+ current levels induced by acidotic pHi. However, block of voltage-gated K+ channels by 3 mmol/l 4-aminopyridine abolished acidosis-induced changes in K+ current amplitudes in both VSM cell types. Interestingly, α-dendrotoxin (100 nmol/l), which blocks only select subtypes of voltage-gated K+ channels, abolished the acidosis-induced decrease in K+current in pulmonary VSM cells but did not affect the acidosis-induced increase in K+ current observed in coronary VSM cells. These findings suggest that opposing, tissue-specific effects of pHi on distinct subtypes of voltage-gated K+ channels in coronary and pulmonary VSM membranes may differentially regulate vascular reactivity in these two circulations under conditions of acidotic stress.

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