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I read with interest the excellent update on adenosine by Polosa and Holgate.1 An important use of this challenge agent is demonstrated and adenosine antagonism as a potential treatment for asthma is revisited. However, the role of adenosine as a mediator of asthma is somewhat inconsistent with several functional observations.
Besides the fact that adenosine has dual effects in many systems, data are available— particularly involving the pharmacology of enprofylline (3-methyl xanthine)—which suggest that the therapeutic efficacy of theophylline (1,3-dimethyl xanthine) in asthma may not reflect adenosine antagonism.2 This latter aspect is significant because theophylline, at therapeutic concentrations, effectively antagonises adenosine (at receptors and functionally in vivo).
Qualitatively different from theophylline, enprofylline does not antagonise the physiological/pathophysiological actions of adenosine2 yet enprofylline and theophylline share several pharmacological actions including cardiac stimulation, microvascular anti-exudative activity, and a range of smooth muscle relaxant effects although enprofylline is consistently about three times more potent than theophylline.2 Equally, enprofylline is about three times more potent than theophylline in asthma as a …