Use of exercise challenge to investigate possible tolerance to beta-adrenoceptor stimulation in asthma

Gibson, Gretchen; Greenacre, J.K.; König, Peter; Conolly, M. E.; Pride, N. B.

doi:10.1016/0007-0971(78)90042-6

Cited by 54 publications

(17 citation statements)

References 17 publications

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“…Several investigations have found an improvement in lung function after the use of high-dose β-agonist therapy, while a substantial number have shown no improvement or evidence of deterioration in lung function consistent with the view that regular β-agonist treatment may be deleterious [42]. Downward trends in baseline lung function during regular treatment with β-agonists are also evident from other studies [49,[51][52][53][54].…”

Section: Do Inhaled β-Agonists Have Adverse Effects On Airways?mentioning

confidence: 62%

“…Although there is no loss of bronchodilator response to β 2 -agonists, several studies have demonstrated loss of protection against various bronchoconstrictor challenges [50,51,55,56], and this may be relevant to the reduced asthma control seen with the regular use of inhaled β 2 -agonists [43,49].…”

Section: Do Inhaled β-Agonists Have Adverse Effects On Airways?mentioning

confidence: 99%

See 1 more Smart Citation

Interactions of glucocorticoids and beta 2-agonists

Adcock

Da²,

Barnes³

1996

Eur Respir J

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Section: Do Inhaled β-Agonists Have Adverse Effects On Airways?mentioning

confidence: 62%

Section: Do Inhaled β-Agonists Have Adverse Effects On Airways?mentioning

confidence: 99%

Interactions of glucocorticoids and beta 2-agonists

Adcock

Da²,

Barnes³

1996

Eur Respir J

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“…In the case of exercise induced bronchospasm a reduction in the protective effect of salbutamol has been demonstrated in six mild asthmatics after between 4 and 20 weeks treatment with oral salbutamol. This effect was not however seen in six adolescents receiving inhaled salbutamol [26].…”

Section: Antibronchoconstrictor Tolerancementioning

confidence: 77%

Tolerance with beta 2‐adrenoceptor agonists: time for reappraisal.

Grove

Lipworth

1995

Brit J Clinical Pharma

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“…The monoclonal antibodies involved in the kit recognize LTC 4 , D 4 , and E 4 equally. 26) The minimal detectable concentration of LT was 12.5 pg/ml.…”

Section: Measurement Of Mediators Releasedmentioning

confidence: 99%

“…Although receptor desensitization is an important mechanism to maintain homeostasis, the same mechanism may interfere with the therapeutic effects of b 2 -adrenoceptor agonists. 4,5) It has been reported that b 2 -adrenoceptor agonists inhibit IgE-mediated release of mediators such as histamine, prostaglandin D 2 (PGD 2 ), and cysteinyl leukotrienes (LT) from human lung fragments, [6][7][8][9] and dispersed human lung and skin mast cells. [10][11][12][13] We also reported that b 2 -adrenoceptor agonists inhibit the chemical mediator release in cultured human mast cells.…”

mentioning

confidence: 99%

Differential Effects of .BETA.2-Adrenoceptor Desensitization on the IgE-Dependent Release of Chemical Mediators from Cultured Human Mast Cells

Tsuji

Kato

Kimata

et al. 2004

Biological & Pharmaceutical Bulletin

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Agonist binding to b 2 -adrenoceptors causes activation of adenylate cyclase through coupling to a stimulatory component of GTP-binding protein (Gs protein) and results in an elevation of intracellular cAMP levels. cAMP plays an important role in inducing cellular responses as a second messenger. It is well known, however, that the responsiveness of b 2 -adrenoceptors wanes after continuous or repeated exposure to the agonists, a phenomenon referred to as desensitization.1-3) The initial step of the desensitization is caused by phosphorylation of intracellular domains of b 2 -adrenoceptors. The receptor phosphorylation results in an uncoupling between receptor proteins and Gs proteins. Two types of protein kinase are considered to be responsible for the phosphorylation. One is a cAMP-dependent protein kinase A (PKA) and the other is a cAMP-independent G proteincoupled receptor kinase such as b 2 -adrenergic receptor kinase (b-ARK). Phosphorylation by b-ARK facilitates the binding of b-arrestin to the receptors, which interferes with the receptor coupling to Gs protein. Prolonged exposure of the receptors to agonists may facilitate the receptor internalization, followed by their degradation. Furthermore, b 2 -adrenoceptor gene expression may be downregulated when cells are exposed continuously to the agonists for a long period. Although receptor desensitization is an important mechanism to maintain homeostasis, the same mechanism may interfere with the therapeutic effects of b 2 -adrenoceptor agonists. 4,5) It has been reported that b 2 -adrenoceptor agonists inhibit IgE-mediated release of mediators such as histamine, prostaglandin D 2 (PGD 2 ), and cysteinyl leukotrienes (LT) from human lung fragments, [6][7][8][9] and dispersed human lung and skin mast cells. [10][11][12][13] We also reported that b 2 -adrenoceptor agonists inhibit the chemical mediator release in cultured human mast cells.14-16) b 2 -Adrenoceptor agonists inhibit mediator release from human mast cells far more potently than disodium cromoglycate. 6,8,13,14) Furthermore, b 2 -adrenoceptor agonists inhibit PGD 2 and LT release more potently than histamine release from human mast cells. 11,13,14) On the other hand, desensitization has also been observed in the inhibition of human mast cell histamine release by b 2 -adrenoceptor agonists. [17][18][19] Chong and Peachell 18) reported that isoproterenol inhibition of histamine release from human lung mast cells is considerably more susceptible to desensitizing treatments than the isoproterenol relaxation of bronchial smooth muscle. In contrast to histamine release, however, desensitization of PGD 2 and LT release inhibition by b 2 -adrenoceptor agonists has rarely been investigated.In the present study therefore, we examined and compared the inhibitory effects of b 2 -adrenoceptor agonists on the release of histamine, PGD 2 , and LT from cultured human mast cells after prolonged treatment with the agonists. Laboratory and Pharmaceutical Research Laboratory, Kirin Brewery Co., Ltd.; Gunma 370-1295 ...

show abstract

Use of exercise challenge to investigate possible tolerance to beta-adrenoceptor stimulation in asthma

Cited by 54 publications

References 17 publications

Interactions of glucocorticoids and beta 2-agonists

Interactions of glucocorticoids and beta 2-agonists

Tolerance with beta 2‐adrenoceptor agonists: time for reappraisal.

Differential Effects of .BETA.2-Adrenoceptor Desensitization on the IgE-Dependent Release of Chemical Mediators from Cultured Human Mast Cells

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