Nicotine in concentration 100 nM which corresponds to concentration of nicotine circulating in tobacco smokes induced hyperpolarization by approximately 4 mV of muscle fibres of the rat isolated diaphragm, as well as an increase in amplitude and acceleration of action potentials. Similar hyperpolarization was induced by nicotine and acetylcholine in the rat soleus muscle. In this muscle, the hyperpolarization developed more slowly than in diaphragm revealing initial slight depolarization. Non-competitive blocker of open channel of nicotinic acetylcholine receptor, proadifen, abolished nicotine- or acetylcholine-induced depolarization but not the hyperpolarization. In the diaphragm, the hyperpolarization was blocked by specific inhibitors of the Na,K-ATPase, ouabain (50 nM) or marinobufagenin (2 nM) suggesting an involvement of the Na,K-ATPase. Estimation of elecrogenic contributions of isoforms of the Na,K-ATPase showed that the hyperpolarization was due to an increase in electrogenic contribution of alpha 2 isoform without change in contribution of alpha 1 isoform. Nicotine did not affect parameters of muscle contractions in response to direct stimulation.
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