Enhancement by glutathione of the inotropic actions of catecholamines and glucagon.
We have previously shown that cardiostimulation produced by catecholamines, glucagon, tachycardia or CaCl2, resulted in a metabolically induced increase in coronary flow [9, 11, 12]. Slow infusion of prostaglandin E2 (PGE2) or its precursor, arachidonic acid, inhibited the development of metabolic coronary dilatation without major alterations of the effects of the cardiostimulating agents on the cardiac activity [9, 11, 12]. Since PGE2 synthesis is known to be enhanced by glutathione we thought that its addition to the perfused heart would intensify the inhibition of the metabolic coronary dilatation produced by arachidonic acid. While testing the influence of noradrenaline in the isolated perfused heart, we found that the inotropic action and the resulting coronary dilatation were markedly increased during glutathione administration. We diverted the investigation from its original purpose to further study this novel action of glutathione and we report here that catecholamines and glucagon inotropic effects, and resulting metabolic coronary dilatation are enhanced by glutathione. Neither the CaCl2 nor the coronary dilatations due to reactive hyperaemia or adenosine were altered by glutathione.
D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects; D004357:Drug Synergism; D005934:Glucagon / Q000494:pharmacology*; D005978:Glutathione / Q000494:pharmacology*; D006168:Guinea Pigs; D009200:Myocardial Contraction / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology*; D051381:Rats; D013268:Stimulation, Chemical
D005934:Glucagon; D005978:Glutathione; D009638:Norepinephrine