TY - JOUR
T1 - α-adrenergic regulation of action potentials in isolated rat cardiomyocytes
AU - Vogel, Stephen M.
AU - Terzic, Andre
PY - 1989/5/19
Y1 - 1989/5/19
N2 - Radioligand binding studies and studies in which inositol phosphate levels were assayed have provided substancial evidence for the existence of α1-adrenoceptors in isolated rat ventricular myocytes, a pure cardiac preparation free of neuronal and vascular elements. Since correlational electrophysiological studies have not been carried out in this model, we investigated α-adrenergic effects on action potentials using intracellular microelectrodes to impale the myocytes. Epinephrine, in the presence of propranolol (10-6 M), rapidly increased the action potential duration in a concentration-dependent manner (threshold concentration of 30 nM, EC50 of 100 nM). The maximal upstroke velocity and overshoot of Ca2+-mediated action potentials (15 mM K+) were also incresed. Epinephrine did not significantly affect the resting membrane potential. The α1-adrenoceptor antagonist, prazosin (10-7 M) blocked epinephrine's effects. LiCl (10 mM), an inhibitor of inositol-phosphate phosphates potentiated the effects of epinephine (30 nM). The results suggest that the isolated rat cardiomyocyte is a suitable preparation for examining the ionic and molecular mechanisms of direct α-adrenergic effects on the cardiac membrane.
AB - Radioligand binding studies and studies in which inositol phosphate levels were assayed have provided substancial evidence for the existence of α1-adrenoceptors in isolated rat ventricular myocytes, a pure cardiac preparation free of neuronal and vascular elements. Since correlational electrophysiological studies have not been carried out in this model, we investigated α-adrenergic effects on action potentials using intracellular microelectrodes to impale the myocytes. Epinephrine, in the presence of propranolol (10-6 M), rapidly increased the action potential duration in a concentration-dependent manner (threshold concentration of 30 nM, EC50 of 100 nM). The maximal upstroke velocity and overshoot of Ca2+-mediated action potentials (15 mM K+) were also incresed. Epinephrine did not significantly affect the resting membrane potential. The α1-adrenoceptor antagonist, prazosin (10-7 M) blocked epinephrine's effects. LiCl (10 mM), an inhibitor of inositol-phosphate phosphates potentiated the effects of epinephine (30 nM). The results suggest that the isolated rat cardiomyocyte is a suitable preparation for examining the ionic and molecular mechanisms of direct α-adrenergic effects on the cardiac membrane.
KW - Cardiac action potential
KW - Epinephrine
KW - Prazosin
KW - α-Adrenoceptors
KW - β-Adrenoceptor blockade
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U2 - 10.1016/0014-2999(89)90463-9
DO - 10.1016/0014-2999(89)90463-9
M3 - Article
C2 - 2547634
AN - SCOPUS:0024338626
SN - 0014-2999
VL - 164
SP - 231
EP - 239
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 2
ER -