DIFFERENCE IN THE ACTIONS OF NICOTINE AND TYRAMINE ON ISOLATED ATRIA

Since the well known hypothesis proposed by Burn and Rand (1) in 1958 that tyramine exerts its sympathomimetic action through release of catecholamine (CA) from its storage sites, there have been many studies on this using various tissues in vitro and in vivo (2-6), and this hypothesis is now generally accepted. Kottegoda (7) found that nicotine first had a negative and then a positive inotropic action on isolated rabbit atrium. This positive inotropic action was not abolished by atropine and Burn and Rand (8) reported that it was also due to the liberation of CA from storage sites. Further, they found that the vasoconstrictor action of nicotine on rabbit ear vessels was also due to the liberation of noradrenaline, since the constrictor action was prevented by injection of reserpine in animals before the experiment, or by removal of the superior cervical ganglion 2 weeks previously (9). Moreover, it was shown that the content of adrenaline in the adrenal gland decreased following nicotine injection (10, 11). However, Kako et al. (12) reported that the CA content in dog heart was slightly increased by the application of nicotine, and Hansson et al. (13) recognized that the CA level in the brain, the heart and the spleen of mice and guinea pigs remained unaffected or possibly slightly elevated in the heart by the injection of nicotine. In addition, other workers (14) observed that nicotine caused an increase in the contractile amplitude of atropinized embryonic chick heart, although the heart was not yet innervated. These facts suggested that the way in which tyramine and nicotine liberate CA from storage sites may differ. In this work, the actions of nicotine and tyramine were compared using isolated atria from normal animals and those treated with reserpine.