Acetylcholine (10(-7)-10(-2) M) enhanced the Na+, K+-ATPase activity in sarcolemmal vesicles from myocardium and intestinal smooth muscle. The stimulation of the enzyme from canine ventricles reaches 150% and was less pronounced (10-20%) in the case of frog myocardium and canine ileal muscles. The activating action of the neurotransmitter was simulated by gramicidin D (1-5 microM), but not by valinomycin 1-5 microM), blocked both by ouabain (200 microM) and atropine (0.1 microM), a muscarinic cholinergic antagonist. The activating action disappeared after treatment of membranes with alamethicin, a pore-producing antibiotic (0.8 mg/mg of protein). It is suggested that an increase in the Na+, K+-ATPase activity caused by acetylcholine is induced by Na+ which permeate the sarcolemmal vesicles through the ionic channel coupled with muscarinic acetylcholine receptor.
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