Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 9594485

Exercise-induced asthma.

L A Wilkerson
View original source ↗Export metadata ↓

Abstract

Exercise-induced asthma is the phenomenon of transient airflow obstruction, typically 5 to 15 minutes after physical exertion. The increased airway resistance produces a 15% or greater decrease in the forced expiratory volume in 1 second, or in peak expiratory flow rate. Exercise-induced asthma occurs in 90% of individuals with asthma, representing 12% to 15% of the population world-wide. The prevalence of exercise-induced asthma among athletes ranges between 3% and 11%. Several theories of the etiology exist: respiratory heat or water loss (or both), hyperventilation causing discharge of bronchospastic chemical mediators or rebound rewarming of the blood in airway tissues. Treatment is either by pharmacologic or nonpharmacologic means, but medication continues to be the cornerstone of therapy for exercise-induced asthma. beta 2-Specific agonists remain the drugs of choice. Cromolyn sodium and nedocromil sodium are alternatives to the beta 2-agonists, and the combined use of the two classes of agents can provide additive benefits.

Explore related subjects

Adrenergic beta-2 Receptor AgonistsAdrenergic beta-AgonistsAdultAnti-Asthmatic AgentsAsthma, Exercise-InducedChildExercise TestHumansMedical History TakingPhysical ExertionPrevalenceRespiratory Function TestsJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

L A Wilkerson. 1998. Exercise-induced asthma.. https://pubmed.ncbi.nlm.nih.gov/9594485/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2003

Antagonism of the antidepressant-like effects of clenbuterol by central administration of beta-adrenergic antagonists in rats.

RATIONALE: Stimulation of central beta(2) adrenergic receptors produces antidepressant-like effects on behavior. At present, it is not known what brain sites are involved in mediating such effects, although some recent evidence suggests the importance of the dorsal hippocampus. OBJECTIVE: Experiments were carried out to determine whether central administration of beta-adrenergic antagonists blocks antidepressant-like effects produced by peripheral administration of the beta(2)-adrenergic agonist clenbuterol. METHODS: The following were determined: 1) the ability of ICV or intrahippocampal administration of the non-selective beta adrenergic antagonists propranolol and CGP-12177, which are lipophilic and hydrophilic, respectively, to antagonize the effects of peripherally administered clenbuterol on differential-reinforcement-of-low-rate (DRL) behavior; 2) the effects of clenbuterol, administered bilaterally into the dorsal hippocampus, on DRL behavior. RESULTS: The antidepressant-like effects of clenbuterol, i.e. reduced response rate and increased reinforcement rate under the DRL schedule, were antagonized by either ICV or bilateral intrahippocampal infusions of propranolol or CGP-12177; CGP-12177 was approximately 8-fold more potent than propranolol. Direct infusion of clenbuterol into the bilateral dorsal hippocampus also produced antidepressant-like effects. CONCLUSIONS: Central beta-adrenergic receptors, in particular those in the dorsal hippocampus, are involved in the mediation of the antidepressant-like effect of clenbuterol. Probably resulting from its enhanced access to the sites of action, the hydrophilic antagonist CGP-12177 was more potent than the lipophilic antagonist propranolol, even though they exhibit similar potency in vitro.

Adrenergic beta-2 Receptor Agonists↗
PubMed2003

PP2A activation by beta2-adrenergic receptor agonists: novel regulatory mechanism of keratinocyte migration.

Understanding the mechanisms that regulate cell migration is important for devising novel therapies to control metastasis or enhance wound healing. Previously, we demonstrated that beta2-adrenergic receptor (beta2-AR) activation in keratinocytes inhibited their migration by decreasing the phosphorylation of a critical promigratory signaling component, the extracellular signal-related kinase (ERK). Here we demonstrate that beta2-AR-induced inhibition of migration is mediated by the activation of the serine/threonine phosphatase PP2A. Pretreating human keratinocytes with the PP2A inhibitor, okadaic acid, prevented the beta2-AR-induced inhibition of migration, either as isolated cells or as a confluent sheet of cells repairing an in vitro "wound" and also prevented the beta2-AR-induced reduction in ERK phosphorylation. Similar results were obtained with human corneal epithelial cells. In keratinocytes, immunoprecipitation studies revealed that beta2-AR activation resulted in the rapid association of beta2-AR with PP2A as well as a 37% increase in association of PP2A with ERK2. Finally, beta2-AR activation resulted in a rapid and transient 2-fold increase in PP2A activity. Thus, we provide the first evidence that beta2-AR activation in keratinocytes modulates migration via a novel pathway utilizing PP2A to alter the promigratory signaling cascade. Exploiting this pathway may result in novel therapeutic approaches for control of epithelial cell migration.

Adrenergic beta-2 Receptor Agonists↗