The acute effects of hydrocortisone on cardiac electrocardiography, action potentials, intracellular calcium, and contraction: The role of protein kinase C

초록

Hydrocortisone exerts adverse effects on various organs, including the heart. This study investigated the still unclear effects of hydrocortisone on electrophysiological and biochemical aspects of cardiac excitation-contraction coupling. In guinea pigs' hearts, hydrocortisone administration reduced the QT interval of ECG and the action potential duration (APD). In guinea pig ventricular myocytes, hydrocortisone reduced contraction and Ca2+ transient amplitudes. These reductions and the effects on APD were prevented by pretreatment with the protein kinase C (PKC) inhibitor staurosporine. In an overexpression system of Xenopus oocytes, hydrocortisone increased hERG K+ currents and reduced Kv1.5 K+ currents; these effects were negated by pretreatment with staurosporine. Western blot analysis revealed dose- and time-dependent changes in PKC alpha/beta II, PKC epsilon, and PKC gamma phosphorylation by hydrocortisone in guinea pig ventricular myocytes. Therefore, hydrocortisone can acutely affect cardiac excitation-contraction coupling, including ion channel activity, APD, ECG, Ca2+ transients, and contraction, possibly via biochemical changes in PKC.

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