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Influence of p2-Adrenergic Receptor Genotype on Airway Function During Exercise in Healthy Adults: Conclusion

Published in Pulmonary Function

Influence of p2-Adrenergic Receptor Genotype on Airway Function During Exercise in Healthy Adults: ConclusionInterestingly, the difference between the Arg16 and Gly16 genotypes in FEF50 occurred during a time when catecholamines were rapidly returning to baseline after the airway P2ARs had been exposed to catecholamines for 10 to 15 min (exercise plus early cool down). This may suggest that significant in vivo desensitization takes between 9 min and 15 min to occur. Garovic et al infused a P-agonist (isoproterenol) at increasing concentrations and measured changes in forearm blood flow in Arg16 and Gly16 homozygotes. http://birthcontroltab.com/buy-alesse-online.html

They found that the Arg16 group had smaller increases in forearm blood flow but did not observe a significant difference between the groups until 6 to 12 min of infusion.
Although a difference in FEF50 between the groups was demonstrated during recovery from exercise, there were no significant differences between the groups in response to a single inhalation of a P-agonist. All subjects followed a standard protocol, which included prebronchodilator spirometry, inhalation of albuterol, followed by a 10 to 15-min rest prior to repeat spirometry. Albuterol is a long-acting P2-selective agonist that has been shown to lead to bronchodilation in a manner that is consistent with exercise-related catecholamine stimulation. The lack of difference between the groups with an inhaled P2-agonist may be due to a slightly shorter time period prior to repeat spirometry (vs exercise), or possibly it is due to different mechanisms of action related to the large endogenous and constant infusion of catecholamines with exercise presumably through the bronchiole circulation vs the effects of a single breath of an inhaled P-agonist.
Both groups had a similar increase in norepinephrine during exercise; however, the Arg16 subjects tended to have a more marked increase in epinephrine during the heavier workload, although not quite reaching significance (p = 0.07). It is possible that the higher epinephrine levels (the primary agonist for the P2AR) may enhance the desensitization in the Arg16 subjects independent of a genotype effect. Both groups did exercise at similar percentage of peak work, for similar time periods, and did not differ in regard to body weight (all factors that could influence epinephrine release). Further study would be needed to determine if there may truly be a genotype-related difference in epinephrine release and if differences in circulating catecholamines may have contributed to the observed differences in expiratory flow after exercise between the groups.