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Response to acetylcholine and nicotine of the perfused vessels of the rabbit ear
Author(s) -
GRAHAM J. D. P.,
SUHAILA A.,
TAI A.
Publication year - 1971
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.1476-5381.1971.tb08047.x
Subject(s) - atropine , acetylcholine , tonic (physiology) , denervation , nicotine , phentolamine , chemistry , endocrinology , vasodilation , medicine , anesthesia , pharmacology , stimulation
Summary1 The vessels of the isolated rabbit ear were perfused at 23 mbar with Krebs solution with (tonic) and without (atonic) noradrenaline (5.9 × 10 −7 M) at selected temperatures of 20°–38° C. Peripheral resistance units (PRU) were calculated from the observed peak flow rates and alterations caused by drugs expressed as Δ% PRU. 2 ACh is constrictor in the atonic vessel. 3 ACh is a vasodilator of the tonic vessel perfused with NA. This effect is potentiated by anticholinesterase and by denervation, unaffected by botulinum toxin and antagonized by atropine. ACh also dilates the vessel perfused with vasopressin. 4 Increasing the temperature reduces the responses to ACh but increases the effect of anticholinesterase. 5 Nicotine causes a dose dependent dilatation of the tonic vessels, reduced but not abolished by C 6 , by atropine, by botulinum toxin and by denervation. 6 Nicotine causes a dose dependent constriction of the atonic vessels, abolished by C 6 and by phentolamine, reduced by denervation, but unaffected by botulinum toxin.