Acidosis counteracts the negative inotropic effect of K+ on ventricular muscle strips from the toad Bufo marinus.
Strenuous activity is associated with acidosis, increased extracellular potassium concentration ([K+]o), and elevated levels of circulating catecholamines. Acidosis and elevated [K+]o are normally considered harmful to cardiac function, and a high sympathetic tone on the heart may lead to arrhythmia. During activity, however, the heart must be able to increase rate and strength of contraction. While the individual effects of [K+]o, acidosis, and adrenaline on contractile properties of cardiac muscle have been characterized for some ectothermic species, less information is available on their interactions. Here we examine the isolated and combined effects of [K+]o, acidosis, and adrenaline on ventricular muscle strips from the toad Bufo marinus. This study showed that increased [K+]o significantly reduced twitch force, while lactic acid significantly increased twitch force and more than counteracted the negative inotropic effects of elevated [K+]o. There was no inotropic effect of Na-lactate (neutralized lactic acid), which suggests that lactic acid stimulated twitch force through reduced pH and not by serving as a substrate. Adrenaline had a positive effect on twitch force in all preparations. Irrespective of treatment, twitch force decreased as stimulation rate increased. During high [K+]o, there was a severe reduction in maximal frequency of toad ventricular strips that was not alleviated by lactic acidosis and/or adrenaline, which suggests that high [K+]o influences twitch force and maximal rate by different mechanisms. In vivo levels of lactic acid, [K+]o, adrenaline, and heart rate previously observed during forced activity in Bufo did not significantly affect the contractile properties of heart muscle strips in vitro. Thus, although [K+]o significantly decreased twitch force, this detrimental effect was more than counteracted by the positive inotropic effect of lactic acid and adrenaline.
Andersen
Johnnie Bremholm
JB
Department of Zoophysiology, Institute of Biological Sciences, University of Aarhus, Universitetsparken, Building 131, DK-8000 Aarhus C, Denmark. johnnie.andersen@biology.au.dk
Gesser
Hans
H
Wang
Tobias
T
D000138:Acidosis / Q000503:physiopathology*; D000704:Analysis of Variance; D000818:Animals; D002024:Bufo marinus / Q000378:metabolism* / Q000502:physiology; D004837:Epinephrine / Q000494:pharmacology; D066298:In Vitro Techniques; D019344:Lactic Acid / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects*; D011188:Potassium / Q000494:pharmacology*; D019289:Pyruvic Acid / Q000494:pharmacology; D019354:Sodium Lactate / Q000494:pharmacology; D013997:Time Factors
D019344:Lactic Acid; D019289:Pyruvic Acid; D011188:Potassium; D019354:Sodium Lactate; D004837:Epinephrine