Altered K+ current profiles underlie cardiac action potential shortening in hyperkalemia and β-adrenergic stimulation

Autor: Leighton T. Izu, Ye Chen-Izu, Bence Hegyi, Tamás Bányász
Rok vydání: 2019
Předmět:
Male
électrophysiologie cellulaire
Hyperkalemia
Physiology
Medical Physiology
Action Potentials
Cardiovascular
physical exercise
2.1 Biological and endogenous factors
Medicine
Myocytes
Cardiac
β adrenergic stimulation
Aetiology
stimulation sympathique
cellular electrophysiology
Cardiac action potential
Pharmacology and Pharmaceutical Sciences
General Medicine
Adrenergic beta-Agonists
potassium channels
Heart Disease
Cardiology
Rabbits
medicine.symptom
Cardiac
medicine.medical_specialty
Heart Ventricles
Physical exercise
heart
arrhythmia
Article
action potential voltage-clamp
Physiology (medical)
Internal medicine
sympathetic stimulation
Animals
hyperkaliémie
Pharmacology
Myocytes
arythmie
business.industry
Isoproterenol
exercice physique
hyperkalemia
cœur
Potassium
business
canaux potassiques
voltage-clamp du potentiel d’action
Zdroj: Can J Physiol Pharmacol
Canadian journal of physiology and pharmacology, vol 97, iss 8
ISSN: 1205-7541
0008-4212
Popis: Hyperkalemia is known to develop in various conditions including vigorous physical exercise. In the heart, hyperkalemia is associated with action potential (AP) shortening that was attributed to altered gating of K+ channels. However, it remains unknown how hyperkalemia changes the profiles of each K+ current under a cardiac AP. Therefore, we recorded the major K+ currents (inward rectifier K+ current, IK1; rapid and slow delayed rectifier K+ currents, IKr and IKs, respectively) using AP-clamp in rabbit ventricular myocytes. As K+ may accumulate at rapid heart rates during sympathetic stimulation, we also examined the effect of isoproterenol on these K+ currents. We found that IK1 was significantly increased in hyperkalemia, whereas the reduction of driving force for K+ efflux dominated over the altered channel gating in case of IKr and IKs. Overall, the markedly increased IK1 in hyperkalemia overcame the relative decreases of IKr and IKs during AP, resulting in an increased net repolarizing current during AP phase 3. β-Adrenergic stimulation of IKs also provided further repolarizing power during sympathetic activation, although hyperkalemia limited IKs upregulation. These results indicate that facilitation of IK1 in hyperkalemia and β-adrenergic stimulation of IKs represent important compensatory mechanisms against AP prolongation and arrhythmia susceptibility.
Databáze: OpenAIRE
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