[Role of nucleoside triphosphatase in the formation of factor-X in frog myocardium following exposure to acetylcholine].
Under the effect of acetylcholine and vagal stimulation on the donor frog myocardium, a uridine polyphosphate-like substance (X-factor) is released. It intensifies contractions of the isolated heart-recipient and decreases the heart's sensitivity to acetylcholine and vagal stimulation. Acetylcholine (1-10(-4)-1-10(-5 g/ml) decreases UTPase activity (by 20-25%) and ATPase activity (by 15%) in isolated ventricle of the frog heart. When acetylcholine is washed away, UTPase activity is almost completely restored. Suppression of UTPase activity by acetylcholine seems to be one of the mechanisms responsible for the accumulation and release and uridine polyphosphates in the heart muscle.
D000109:Acetylcholine / Q000494:pharmacology; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D001001:Anura; D006321:Heart / Q000294:innervation; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism*; D011433:Propranolol / Q000494:pharmacology; D011755:Pyrophosphatases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D011896:Rana temporaria; D012969:Sodium Fluoride / Q000494:pharmacology; D014500:Uracil Nucleotides / Q000096:biosynthesis*; D014630:Vagus Nerve / Q000502:physiology
D014500:Uracil Nucleotides; D012969:Sodium Fluoride; D011433:Propranolol; D000251:Adenosine Triphosphatases; D011755:Pyrophosphatases; D000109:Acetylcholine
Rol' nucleozidtrifosfatazy v obrazovanii X-faktora v miokarde liagushki pri deĭstvii atsetilkholina.