Glycogenolysis in the heart and skeletal muscle during stimulation and blocking of cholinergic receptors. II. Action of cholinolytic compounds.
In Part I of this study it was found that slow injection of acetylcholine causes an increase in phosphorolytic activity in the working heart and resting skeletal muscle, and at the same time decreases hydrolytic activity. At present, it is shown that atropine and tubocurarine do not inhibit this activity of acetylcholine, but that it is inhibited by blocking the N1 receptor with hexamethonium. These findings indicate that neither the muscarinic receptor in the heart nor the nicotinic N2 receptor in skeletal muscle take part in regulation of glycogenolysis, which is connected with the action of acetylcholine on the cholinergic N1 receptor. Ganglioplegic compounds stimulate hydrolytic activity (hexamethonium, atropine in large doses).
D000109:Acetylcholine / Q000494:pharmacology; D000249:Adenosine Monophosphate / Q000378:metabolism; D000818:Animals; D006003:Glycogen / Q000378:metabolism*; D006868:Hydrolysis; D008297:Male; D009132:Muscles / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D010276:Parasympatholytics / Q000494:pharmacology*; D051381:Rats; D011950:Receptors, Cholinergic / Q000187:drug effects*; D014403:Tubocurarine / Q000494:pharmacology
D010276:Parasympatholytics; D011950:Receptors, Cholinergic; D000249:Adenosine Monophosphate; D006003:Glycogen; D000109:Acetylcholine; D014403:Tubocurarine