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NICOTINE STIMULATES PROSTAGLANDIN FORMATION IN THE RABBIT HEART
Author(s) -
WENNMALM Å.
Publication year - 1977
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.1476-5381.1977.tb06981.x
Subject(s) - atropine , nicotine , acetylcholine , chemistry , prostaglandin , pharmacology , nicotinic agonist , receptor , endocrinology , medicine , biochemistry
1 Rabbit isolated hearts were perfused according to Langendorff with Tyrode solution. Prostaglandin‐like substances (PLS) in the effluent were purified and assayed on the rat stomach strip. Noradrenaline (NA) in the effluent was assayed fluorimetrically. 2 Infusion of nicotine (1 μ m ‐50 μ m ) caused a dose‐dependent, brief increase, from 1.2 ± 0.4 to maximally 8.3 ± 2.1 ng/min, in the outflow of PLS from the heart. The increase was abolished by pretreatment of the heart with indomethacin. 3 Activation of nicotinic receptors in the heart with acetylcholine (ACh, 200 μ m ) in the presence of atropine (1 μ m ) also elicited an increase in the release of PLS. This release was smaller than that caused by nicotine. 4 Nicotine (50 μ m ) and ACh (200 μ m ) in the presence of atropine (1 μ m ) each caused a pronounced but brief release of NA into the effluent. There was no evident correlation between the ability of the drugs to cause release of PLS on the one hand, and NA on the other. 5 It is concluded that nicotine acts as a direct stimulus for the synthesis of prostaglandins in the rabbit heart.