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Hypothermia‐induced supersensitivity to adenosine for responses mediated via A 1 receptors but not A 2 ‐receptors
Author(s) -
Broadley Kenneth J.,
Broome Shelley,
Paton David M.
Publication year - 1985
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1985.tb12924.x
Subject(s) - receptor , adenosine , adenosine receptor , hypothermia , neuroscience , chemistry , pharmacology , medicine , biology , agonist
1 Four isolated tissues were examined in which the responses to adenosine are mediated via either A 1 ‐or A 2 ‐receptors. 2 The responses examined were the inhibition of cholinergic transmission of field‐stimulated guinea‐pig ileum (A 1 ), inhibition of noradrenergic transmission of field‐stimulated rat vas deferens (A 1 ), inhibition of developed tension of rat paced left atria (A 1 ) and relaxation of carbachol‐contracted guinea‐pig trachea (A 2 ). 3 Cumulative concentration‐response curves for adenosine and 2‐chloroadenosine were constructed at 37, 30 or 27°C. 4 When plotted as a percentage of the maximum response, the concentration‐response curves were displaced to the left by cooling in the ileum, vas deferens and atria, indicative of supersensitivity. 5 This increase in sensitivity does not arise from inhibition of uptake or deamination by cooling, since it occurs equally for adenosine and 2‐chloroadenosine, the latter being immune to these processes. 6 In contrast, the sensitivity of the trachea was not affected (2‐chloroadenosine) or reduced (adenosine) by cooling. 7 Thus responses mediated via adenosine receptors of the A 1 subtype exhibit hypothermia‐induced supersensitivity, whereas those mediated via A 2 ‐receptors do not. This suggests a fundamental temperature‐dependent difference between the two adenosine receptor subtypes.