Oxidative Stress and Receptor Responses in Guinea-Pig Tracheal Tissue

1990 ◽  
pp. 143-145
Author(s):  
Cees J. A. Doelman ◽  
Janneke F. de Vlieger ◽  
R. Corinne Sprong ◽  
Aalt Bast
Keyword(s):  
Oxidative Stress ◽  
Guinea Pig ◽  
Tracheal Tissue

HOCl causes airway substance P hyperresponsiveness and neutral endopeptidase hypoactivity

1990 ◽  
Vol 258 (6) ◽  
pp. L361-L368 ◽  
Author(s):  
C. G. Murlas ◽  
T. P. Murphy ◽  
Z. Lang
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Muscle Force ◽  
Hypochlorous Acid ◽  
Neutral Endopeptidase ◽  
Krebs Solution ◽  
Solution Ph ◽  
Reverse Phase ◽  
Tracheal Tissue

We investigated whether exposure of guinea pig tracheal tissue to hypochlorous acid (HOCl) or hydrogen peroxide (H2O2) by perfusion through the airway lumen affected the responsiveness of airway muscle to ACh, KCl, or substance P in the presence or absence of 1 microM phosphoramidon, an inhibitor of neutral endopeptidase (NEP). Pairs of tracheal segments were immersed in a Krebs solution (pH 7.40 at 37 degrees C) and connected to perfusion circuits so that the lumen of one segment of each pair could be perfused with Krebs solution while the other was perfused for the same time (10 min) with either 0.1 microM HOCl or 10 mM H2O2. Segments after perfusion were cut into rings of similar size and placed in muscle chambers so that airway muscle force generation in vitro could be measured on stimulation by cumulative agonist doses. In addition, cell homogenates were made from other, similarly perfused tracheal segments to assess NEP activity using reverse-phase, high-pressure liquid chromatography (HPLC). We found that smooth muscle of mucosa-intact guinea pig airways perfused with HOCl, but not H2O2, was hyperresponsive to substance P but not to ACh or KCl. HOCl-perfused rings were not different from Krebs solution-exposed rings pretreated with phosphoramidon. There was no increase in substance P responsiveness of HOCl-exposed airways in which the mucosa had been removed before testing in vitro. The substance P hyperresponsiveness of HOCl-exposed, mucosa-intact airways was associated with decreased NEP activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Cav1.2 calcium channel is glutathionylated during oxidative stress in guinea pig and ischemic human heart

2011 ◽  
Vol 51 (8) ◽  
pp. 1501-1511 ◽  
Author(s):  
Helen Tang ◽  
Helena M. Viola ◽  
Aleksandra Filipovska ◽  
Livia C. Hool
Keyword(s):  
Oxidative Stress ◽  
Guinea Pig ◽  
Calcium Channel ◽  
Human Heart

scholarly journals Prenatal vitamin C deficiency results in differential levels of oxidative stress during late gestation in foetal guinea pig brains

Redox Biology ◽  
2014 ◽  
Vol 2 ◽  
pp. 361-367 ◽  
Author(s):  
Maya D. Paidi ◽  
Janne G. Schjoldager ◽  
Jens Lykkesfeldt ◽  
Pernille Tveden-Nyborg
Keyword(s):  
Oxidative Stress ◽  
Vitamin C ◽  
Guinea Pig ◽  
Late Gestation ◽  
Vitamin C Deficiency

407 ETHANOL CONSUMPTION INCREASES SYSTEMIC OXIDATIVE STRESS IN THE GRAVID GUINEA PIG

2005 ◽  
Vol 53 (1) ◽  
pp. S325.5-S325
Author(s):  
P. Young ◽  
X. D. Ping ◽  
L. A.S. Brown ◽  
T. W. Gauthier
Keyword(s):  
Oxidative Stress ◽  
Guinea Pig ◽  
Ethanol Consumption ◽  
Systemic Oxidative Stress

scholarly journals Novel airway smooth muscle–mast cell interactions and a role for the TRPV4-ATP axis in non-atopic asthma

2020 ◽  
Vol 56 (1) ◽  
pp. 1901458 ◽  
Author(s):  
Sara J. Bonvini ◽  
Mark A. Birrell ◽  
Eric Dubuis ◽  
John J. Adcock ◽  
Michael A. Wortley ◽  
...  
Keyword(s):  
Mast Cell ◽  
Smooth Muscle ◽  
Mast Cells ◽  
Guinea Pig ◽  
Airway Smooth Muscle ◽  
Cell Activation ◽  
Transient Receptor Potential ◽  
Atopic Asthma ◽  
Mast Cell Activation ◽  
Tracheal Tissue

Mast cell–airway smooth muscle (ASM) interactions play a major role in the immunoglobulin (Ig)E- dependent bronchoconstriction seen in asthma but less is known about IgE-independent mechanisms of mast cell activation. Transient receptor potential cation channel, subfamily V, member 4 (TRPV4) activation causes contraction of human ASM via the release of cysteinyl leukotrienes (cysLTs) but the mechanism is unknown. The objective of the present study was to investigate a role for IgE-independent, mast cell–ASM interaction in TRPV4-induced bronchospasm.Bronchoconstriction was measured in anaesthetised guinea pigs and contraction of human and guinea-pig airway tissue assessed using isometric tension measurements. Increases in intracellular [Ca2+] were imaged using the Ca2+-sensitive dye FURA2, and time-lapse ptychography was utilised as a surrogate for contraction of ASM cells.The TRPV4 agonist GSK1016790A caused contraction in vivo in the guinea pig, and in human and guinea-pig tracheal tissue, which was inhibited by the TRPV4 antagonist GSK2193874. GSK1016790A increased [Ca2+]i and released ATP in human ASM cells without causing contraction. TRPV4 and ATP evoked contraction in isolated tracheal tissue but co-culture experiments indicated a requirement for human lung mast cells. Expression profiling and pharmacological studies demonstrated that mast cell activation was dependent upon ATP activating the P2X4 receptor. Trypsin was shown to evoke contraction of tracheal tissue via activation of PAR-2-TRPV4-ATP-cysLT axis indicating the potential disease relevance of this signalling pathway.TRPV4 activation increases [Ca2+]i and releases ATP from ASM cells triggering P2X4-dependent release of cysLTs from mast cells resulting in ASM contraction. This study delineates a novel mast cell–ASM interaction and TRPV4 as a driver of IgE-independent mast cell-dependent bronchospasm.

Increased cholinergic antagonism underlies impaired beta-adrenergic response in ovalbumin-sensitized guinea pigs

1993 ◽  
Vol 74 (6) ◽  
pp. 2729-2735 ◽  
Author(s):  
M. Wills-Karp ◽  
M. I. Gilmour
Keyword(s):  
Guinea Pig ◽  
Intrinsic Defect ◽  
Muscarinic Agonist ◽  
Muscarinic Agonists ◽  
Beta Adrenergic ◽  
Beta Adrenoceptor ◽  
Adrenergic Response ◽  
Cholinergic Pathway ◽  
Tracheal Tissue ◽  
And Control

The goal of this study was to determine if the hyporesponsiveness to beta-adrenoceptor stimulation observed in ovalbumin-sensitized tracheal smooth muscle is due to increased cholinergic muscarinic tone or to a defect in the beta-adrenergic cascade itself. We examined the effects of ovalbumin-sensitization on the responsiveness of guinea pig tracheae to agents that mediate relaxation at various steps in the beta-adrenergic cascade when the tracheal tissue was preconstricted with either carbachol or histamine. Ovalbumin sensitization caused significant reductions in the maximal relaxations both to the beta-adrenergic agonist isoproterenol and to prostaglandin E2 (PGE2) in guinea pig trachealis when the tracheal tissue was preconstricted with the muscarinic agonist carbachol. In contrast, sensitization had no effect on the ability of PGE2 and isoproterenol to relax histamine contractions. Preconstricting the tissues with increasing concentrations of KCl reduced the effectiveness of isoproterenol to relax equally airway tissues from both sensitized and control animals. Forskolin-induced relaxations of trachealis muscle were not altered with sensitization. When tracheal tissues were precontracted with increasing concentrations of carbachol, the effectiveness of isoproterenol and PGE2 to relax airway tissues decreased. Functional antagonism of relaxations by muscarinic agonists was enhanced in the sensitized tissues, since the concentration of carbachol necessary to reduce beta-adrenoceptor-induced relaxations to the same degree as in the control animals was a log dose lower. These results suggest that the impaired beta-adrenoceptor response in sensitized tissues is not due to an intrinsic defect in the beta-adrenergic cascade but to an enhancement of a muscarinic cholinergic pathway.

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