The effect of harmaline on membrane potentials of rat atrial contractile fibers.
Rat atria either beating spontaneously or electrically driven were were perfused in vitro at 30 degrees C. When the preparations were exposed to harmaline 8.3 x 10(-5) or 16.6 x 10(-5) M the atrial rate showed down and the following changes in membrane potentials were observed: (1) a transient increase in the amplitude of the action potential (AAP), in the absence of any change in the magnitude of the resting potential (RP), followed by a progressive decrease of AaP; (2) a progressive decline of the slope of the fast ascending phase of the action potential, which was initially independent of any change in the magnitude of the rp; (3) a progressive increase of the duration of the action potential; (4) a fall in the magnitude of the resting potential. The conclusions proposed are that harmaline: (1) stimulates the slow current responsible for the last part of the upstroke and the beginning of the repolarization; (2) inhibits the sodium current responsible for the fast component of the upstroke; (3) slows doen the processes responsible for the repolarization; (4) inhibits the (Na+-K+) activated membrane ATPase.
D000200:Action Potentials / Q000187:drug effects; D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors; D000470:Alkaloids / Q000494:pharmacology*; D000818:Animals; D016275:Atrial Function; D006246:Harmaline / Q000494:pharmacology*; D006325:Heart Atria / Q000201:enzymology; D006339:Heart Rate / Q000187:drug effects; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects*; D009474:Neurons / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium; D051381:Rats; D012964:Sodium
D000470:Alkaloids; D012964:Sodium; D006246:Harmaline; D000251:Adenosine Triphosphatases; D011188:Potassium; D009638:Norepinephrine