ATROPINE MODIFIES EFFECTS OF ACETYLCHOLINE ON SLOW INWARD CALCIUM CURRENT OF FROG ATRIUMстатья
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Дата последнего поиска статьи во внешних источниках: 26 февраля 2018 г.
Аннотация:The ability of acetylcholine to decrease slow inward calcium current (I(Ca)) in frog atrial cells by activating muscarinic cholinergic receptors (M-ChR) has been well documented. It is generally accepted that atropine is a simple competitive antagonist of M-ChR without any other physiological effects. However, recent reports indicate that atropine (1-mu-M) is capable of increasing I(Ca) (measured by the double sucrose gap technique) by 20-25% above the control value. This effect is more pronounced (50%) after a 15-20 - min pretreatment in the presence of a nonhydrolyzable GTP analogue, 5'-guanylimidodiphosphate (Gpp[NH]p) (5-10-mu-M).
In the presence of Gpp[NH]p and isoproterenol (1-mu-M) an increase of I(Ca) induced by atropine is less pronounced than in the presence of Gpp[NH]p alone. In similar conditions acetylcholine causes an ordinary inhibitory effect.
It has been shown that atropine not only stimulates I(Ca) but also modifies the acetylcholine effect on this current. When atropine is applied after the pretreatment of trabeculae with Gpp[NH]p and isoproterenol, the subsequent acetylcholine addition induces a significant increase of I(Ca) (by 50-100% in different experiments). Similar results have been obtained with another antagonist of M-ChR, scopolamine.
The results obtained can be interpreted in terms of a model of two interconvertible forms of muscarinic cholinergic receptor with the preferential affinity towards either agonist or antagonist. It is proposed that atropine can stabilize the muscarinic receptors in physiologically active state and produced biological effects opposite to those of agonists.