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Effect of hypothermia on β 1 ‐adrenoceptor‐mediated relaxation of pig bronchus
Author(s) -
Foster Paul S.,
Goldie Roy G.,
Paterson James W.,
Spina Domenico
Publication year - 1983
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.1476-5381.1983.tb10060.x
Subject(s) - fenoterol , isoprenaline , orciprenaline , potency , phenoxybenzamine , hypothermia , chemistry , bronchodilatation , endocrinology , bronchus , medicine , catecholamine , guinea pig , pharmacology , biology , bronchodilator , lung , receptor , biochemistry , asthma , in vitro , respiratory disease , stimulation
1 The relaxant potencies of (±)‐isoprenaline and of (−)‐noradrenaline (NA) in the pig isolated bronchus were increased 5.4 and 3.1 fold respectively by lowering the organ bath temperature from 37°C to 27°C, whereas the potencies of the non‐catecholamine β‐adrenoceptor agonists fenoterol and orciprenaline were not significantly changed. 2 At 37°C, the catechol‐ O ‐methyl transferase (COMT) inhibitor U‐0521 (30 μ m ), caused a 7.2 fold increase in the potency of isoprenaline but had no effect on the potency of fenoterol. At 27°C the potency of isoprenaline was similar in the absence or presence of U‐0521 (30 μ m ). Furthermore, in bronchi where extraneuronal uptake was inhibited by phenoxybenzamine, the potency of NA was not significantly altered by reducing bathing temperature from 37°C to 27°C. 3 These results suggest that the hypothermic potentiation of isoprenaline in pig bronchus resulted from inhibition of COMT or of access to COMT, rather than from sensitization of β 1 ‐adrenoceptors.