Agonist-independent alteration in β-adrenoceptor-G-protein-adenylate cyclase system in an equine model of recurrent airway obstruction

Abraham, Getu; Kottke, Claudia; Dhein, Stefan; Ungemach, F. R.

doi:10.1016/j.pupt.2005.05.007

Cited by 13 publications

(10 citation statements)

References 49 publications

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“…In addition, on equine carbachol precontracted tracheal strips, we have provided evidence that Ssalbutamol had a modest, but significant, bronchoconstrictor effect [13,18]. These data may support the deleterious role of S-salbutamol, particularly in RAO-affected horses, in which the β 2 -adrenergic receptor-G s -protein-adenylate cyclase system is significantly impaired in membranes of peripheral lung and bronchi, when compared with the segments from control animals [19].…”

Section: Discussionmentioning

confidence: 53%

“…Thus it has been reported that Ssalbutamol potentiates the pro-constrictory activity of histamine and IL-4 in sensitized guinea pigs [24], by stimulating the production of IL-2 and IL-13 in T-cells [25]. Over all, these cytokines shift the coupling of the β 2 -adrenergic receptors to pro-constrictory G proteins such as G iα-1 protein [19]. Considering all these data, it is possible to hypothesize an analogous pro-inflammatory and pro-constrictory activity of S-salbutamol also in equine airways after only 90 min.…”

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

Evaluation of the effects of the R- and S-enantiomers of salbutamol on equine isolated bronchi

Matera¹,

Calzetta²,

Rogliani³

et al. 2011

Pulmonary Pharmacology & Therapeutics

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Section: Discussionmentioning

confidence: 53%

Section: Discussionmentioning

confidence: 98%

Evaluation of the effects of the R- and S-enantiomers of salbutamol on equine isolated bronchi

Matera¹,

Calzetta²,

Rogliani³

et al. 2011

Pulmonary Pharmacology & Therapeutics

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“…A similar anti-inflammatory effect was found in both conditions, indicating no desensitization of receptors on inflammatory cells occurred in this model. Thus, other mechanisms may be responsible for the reduction of the effectiveness of both bronchodilators during the course of repeated cadmium administration, such as the down-regulated expression of β-adrenoceptors with the progression of the disease as documented in patients with COPD (Zhu et al, 2008) and the impairment of β-adrenoceptor-G(S)-protein-adenylate cyclase system as described by Abraham et al (Abraham et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Effects of formoterol and ipratropium bromide on repeated cadmium inhalation-induced pulmonary inflammation and emphysema in rats

Zhang

Fiévez

Zhang

et al. 2010

European Journal of Pharmacology

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The anti-inflammatory properties of inhaled formoterol and ipratropium bromide, alone or in combination, were investigated in a rat model of chronic pulmonary inflammation with airspace enlargement induced by cadmium inhalation. At the end of the protocol, cadmium-induced increase of airway resistance was prevented by formoterol (4 mg/30 ml) or ipratropium (0.20 mg/20 ml). Formoterol elicited a significant decrease in total cell and neutrophil counts in bronchoalveolar lavage fluid as well as on the activity of gelatinase B (MMP-9), an enzyme strongly expressed in alveolar macrophages and epithelial cells. Additionally, a significant attenuation of the lung lesions characterized by inflammatory cell infiltration within the alveoli and the interstitium and a decrease in mean linear intercept were observed. Although ipratropium alone had no effects on the cadmium-induced pulmonary inflammation and emphysema, its combination with an inefficient concentration of formoterol (1 mg/30 ml) showed a synergistic inhibitory effect on neutrophil and total cell counts as well as on the mean linear intercept associated with a synergistic inhibition on the MMP-9 activity. Gelatinase A (MMP-2) activity was not influenced by drug pretreatments. Neither macrophage metalloelastase (MMP-12) activity nor levels of cytokines IL-1β, TNF-α and GM-CSF in bronchoalveolar lavage fluid were modified in rats chronically exposed to cadmium. No desensitization of β 2 -adrenoceptors or cholinergic receptors on airway smooth muscles and inflammatory cells during the protocol was observed. In conclusion, formoterol alone or combined with ipratropium bromide partially protects the lungs against the chronic inflammation and airspace enlargement by reducing neutrophilic infiltration possibly via the inhibition of MMP-9 activity.

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“…The high susceptibility of b 2 -adrenoceptors located on inflammatory cells to desensitization may be explained by several reasons. Other mechanisms may not be excluded, such as the downregulated expression of b-adrenoceptors in the inflammatory cells with the progression of the disease in patients with COPD and the impairment of b-adrenoceptor-G S -adenylate cyclase system [67,68]. Other mechanisms may not be excluded, such as the downregulated expression of b-adrenoceptors in the inflammatory cells with the progression of the disease in patients with COPD and the impairment of b-adrenoceptor-G S -adenylate cyclase system [67,68].…”

Section: Anti-inflammatory Effects Of Labas and Sabasmentioning

confidence: 99%

Can β₂‐adrenoceptor agonists, anticholinergic drugs, and theophylline contribute to the control of pulmonary inflammation and emphysema in COPD?

Zhang

Cui

et al. 2011

Fundamemntal Clinical Pharma

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Chronic obstructive pulmonary disease (COPD) has become a global epidemic disease with an increased morbidity and mortality in the world. Inflammatory process progresses and contributes to irreversible airflow limitation. However, there is no available therapy to better control the inflammatory progression and therefore to reduce the exacerbations and mortality. Thus, the development of efficient anti-inflammatory therapies is a priority for patients with COPD. β(2) -Adrenoceptor agonists and anticholinergic agents are widely used as first line drugs in management of COPD because of their efficient bronchodilator properties. At present, many studies in vitro and some data obtained in laboratory animals reveal the potential anti-inflammatory effects of these bronchodilators but their protective role against chronic inflammation and the development of emphysema in patients with COPD remains to be investigated. The anti-inflammatory effects of theophylline at low doses have also been identified. Beneficial interactions between glucocorticoids and bronchodilators have been reported, and signaling pathways explaining these synergistic effects begin to be understood, especially for theophylline. Recent data demonstrating interactions between anticholinergics with β(2) -adrenoceptor agonists aiming to better control the pulmonary inflammation and the development of emphysema in animal models of COPD justify the priority to investigate the interactive effects of a tritherapy associating corticoids with the two main categories of bronchodilators.

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Agonist-independent alteration in β-adrenoceptor-G-protein-adenylate cyclase system in an equine model of recurrent airway obstruction

Cited by 13 publications

References 49 publications

Evaluation of the effects of the R- and S-enantiomers of salbutamol on equine isolated bronchi

Evaluation of the effects of the R- and S-enantiomers of salbutamol on equine isolated bronchi

Effects of formoterol and ipratropium bromide on repeated cadmium inhalation-induced pulmonary inflammation and emphysema in rats

Can β₂‐adrenoceptor agonists, anticholinergic drugs, and theophylline contribute to the control of pulmonary inflammation and emphysema in COPD?

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Agonist-independent alteration in β-adrenoceptor-G-protein-adenylate cyclase system in an equine model of recurrent airway obstruction

Cited by 13 publications

References 49 publications

Evaluation of the effects of the R- and S-enantiomers of salbutamol on equine isolated bronchi

Evaluation of the effects of the R- and S-enantiomers of salbutamol on equine isolated bronchi

Effects of formoterol and ipratropium bromide on repeated cadmium inhalation-induced pulmonary inflammation and emphysema in rats

Can β2‐adrenoceptor agonists, anticholinergic drugs, and theophylline contribute to the control of pulmonary inflammation and emphysema in COPD?

Contact Info

Product

Resources

About

Can β₂‐adrenoceptor agonists, anticholinergic drugs, and theophylline contribute to the control of pulmonary inflammation and emphysema in COPD?