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Your search keyword '"Bronchoconstrictor Agents"' showing total 4 results
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4 results on '"Bronchoconstrictor Agents"'

1. The differential roles of the two NO-GC isoforms in adjusting airway reactivity

Author

Malte Verheyen, Michelle Puschkarow, Stefanie Gnipp, Doris Koesling, Marcus Peters, and Evanthia Mergia

Subjects
Mice, Knockout, Pulmonary and Respiratory Medicine, Ovalbumin, Physiology, Vasodilator Agents, Heme, Cell Biology, Nitric Oxide, Bronchoconstrictor Agents, Mice, Soluble Guanylyl Cyclase, Guanylate Cyclase, Physiology (medical), Animals, Protein Isoforms, Cyclic GMP, Methacholine Chloride
Abstract

The enzyme, nitric oxide-sensitive guanylyl cyclase (NO-GC), is activated by binding NO to its prosthetic heme group and catalyzes the formation of cGMP. The NO-GC is primarily known to mediate vascular smooth muscle relaxation in the lung, and inhaled NO has been successfully used as a selective pulmonary vasodilator. In comparison, NO-GC’s impact on the regulation of airway tone is less acknowledged and, most importantly, little is known about the issue that NO-GC signaling is accomplished by two isoforms: NO-GC1 and NO-GC2, implying the existence of distinct “cGMP pools.” Herein, we investigated the functional role of the NO-GC isoforms in respiration by measuring lung function parameters of isoform-specific knockout (KO) mice using noninvasive and invasive techniques. Our data revealed the participation and ongoing influence of NO-GC1-derived cGMP in the regulation of airway tone by showing that respiratory resistance was enhanced in NO-GC1-KOs and increased more pronouncedly after the challenge with the bronchoconstrictor methacholine. The tissue resistance and stiffness of NO-GC1-KOs were also higher because of narrowed airways that cause tissue distortion. Contrariwise, NO-GC2-KOs displayed reduced tissue elasticity, elastic recoil, and airway reactivity to methacholine, which did not even increase in an ovalbumin model of asthma that induced hyperresponsiveness in NO-GC1-KOs. In addition, conscious NO-GC2-KOs showed a higher breathing rate with a shorter duration of inspiration and expiration time, which remained faster even in the presence of bronchoconstrictors that slow down breathing. Thus, we provide evidence of two distinct NO/cGMP pathways in airways, accomplished by either NO-GC1 or NO-GC2, adjusting differentially the airway reactivity.

Published
2022
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3. Airway Smooth Muscles Contractions in Metabolic Syndrome

Author

Yu G, Birulina, V V, Ivanov, E E, Buiko, A N, Dzyuman, A V, Nosarev, O V, Voronkova, M O, Vol'khina, and S V, Gusakova

Subjects
Bronchoconstrictor Agents, Metabolic Syndrome, Carbohydrates, Animals, Albuterol, Bronchi, Carbachol, Muscle, Smooth, Receptors, Cholinergic, Muscle Contraction, Rats
Abstract

We studied contractile responses of isolated airway smooth muscle segments from rats with metabolic syndrome. Metabolic syndrome was induced in rats by high-fat and high-carbohydrate diet. It was shown that metabolic syndrome was associated with an increase of bronchoconstrictor action of cholinergic receptor activator carbacholine (0.1-100 μM) and a decrease of the dilatory effect of β

Published
2022

4. The differential roles of the two NO-GC isoforms in adjusting airway reactivity.

Author

Verheyen M, Puschkarow M, Gnipp S, Koesling D, Peters M, and Mergia E

Subjects
Animals, Cyclic GMP metabolism, Heme, Methacholine Chloride pharmacology, Mice, Mice, Knockout, Nitric Oxide metabolism, Ovalbumin, Protein Isoforms metabolism, Soluble Guanylyl Cyclase metabolism, Vasodilator Agents, Bronchoconstrictor Agents, Guanylate Cyclase metabolism
Abstract

The enzyme, nitric oxide-sensitive guanylyl cyclase (NO-GC), is activated by binding NO to its prosthetic heme group and catalyzes the formation of cGMP. The NO-GC is primarily known to mediate vascular smooth muscle relaxation in the lung, and inhaled NO has been successfully used as a selective pulmonary vasodilator. In comparison, NO-GC's impact on the regulation of airway tone is less acknowledged and, most importantly, little is known about the issue that NO-GC signaling is accomplished by two isoforms: NO-GC1 and NO-GC2, implying the existence of distinct "cGMP pools." Herein, we investigated the functional role of the NO-GC isoforms in respiration by measuring lung function parameters of isoform-specific knockout (KO) mice using noninvasive and invasive techniques. Our data revealed the participation and ongoing influence of NO-GC1-derived cGMP in the regulation of airway tone by showing that respiratory resistance was enhanced in NO-GC1-KOs and increased more pronouncedly after the challenge with the bronchoconstrictor methacholine. The tissue resistance and stiffness of NO-GC1-KOs were also higher because of narrowed airways that cause tissue distortion. Contrariwise, NO-GC2-KOs displayed reduced tissue elasticity, elastic recoil, and airway reactivity to methacholine, which did not even increase in an ovalbumin model of asthma that induced hyperresponsiveness in NO-GC1-KOs. In addition, conscious NO-GC2-KOs showed a higher breathing rate with a shorter duration of inspiration and expiration time, which remained faster even in the presence of bronchoconstrictors that slow down breathing. Thus, we provide evidence of two distinct NO/cGMP pathways in airways, accomplished by either NO-GC1 or NO-GC2, adjusting differentially the airway reactivity.

Published
2022
Full Text
View/download PDF

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