Effects of alpha adrenergic stimulations and blockade on early afterdepolarizations induced by cesium in canine cardiac Purkinje fibers

S. Kaseda, D. P. Zipes

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Abstract

The effects of alpha adrenergic stimulation and three alpha adrenoceptor blockers on early afterdepolarizations (EADs) were examined in canine card diac Punkinje fibers. In the first group of 18 preparations, EADs were induced by superfusion with 7.5 mM cesium (Cs) dissolved in low potassium (2.7 mM KCI) Tyrode's solution. During alpha adrenoceptor stimulation (norepinephrine 1μM and propranolol 1μM) to enhance EADs, the effects of phentolamine and two new alpha 1 adrenoceptor antagonists, benoxathian and WB 4101 (1,3, and 10μM), were examined. WB 4101 (1μM) suppressed EADs in all six preparations. Benoxathian required 3μM in five preparations and 10 μM in one to suppress EADs. Phentolamine (10μM) suppressed EADs in two of six preparations. In the second group of 21 preparations, the effects on cesium-induced EADs of the three alpha adrenoceptor blockers (10μM) were examined without alpha adrenoceptor stimulation. WB 4101 (10μM) suppressed EADs in seven of seven preparations, while benoxathian (10μM) suppressed EADs in five of seven. Phentolamine (10μM) enhanced EADs in six of seven preparations. In the third group of 24 Purkinje fibers, the direct effects (without alpha adrenoceptor stimulation) of these three antagonists on the characteristics of normal Punkinje fiber action potentials superfused with normal Tyrode's solution were examined. Phentolamine (1,3, and 10μM, n = 8) prolonged action potential duration at 90% repolarization (APD90) by 5.3%±1.3%, 10.0% ± 1.8%, and 14.3% ± 2.7%, respectively. Benoxathian (n = 8) and WB 4101 (n = 8) shortened APD90 equally: 6.8% ± 1.1% vs 7.7% ± 1.3% at 1 μM, 13.6% ± 1.0% vs 14.5% ± 1.6% at 3 μM, and 21.1% ± 1.2% vs 20.8% ± 2.1% at 10μM, respectively. We conclude that in cesium treated Purkinje fibers: (1) Alpha adrenoceptor stimulation enhanced EADs; (2) Phentolamine was least effective in suppressing EADs, probably because of a direct effect that prolonged APD90; and (3) Although benoxathian and WB 4101 had similar effects on APD90, WB 4101 was more effective in suppressing EADs at lower concentations than benoxathian.

Original languageEnglish
Pages (from-to)31-40
Number of pages10
JournalJournal of Cardiovascular Electrophysiology
Volume1
Issue number1
StatePublished - 1990

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Purkinje Fibers
Cesium
Adrenergic Agents
Adrenergic Receptors
Canidae
Phentolamine
Action Potentials
Propranolol
benoxathian
(2-(2',6'-dimethoxy)phenoxyethylamino)methylbenzo-1,4-dioxane
Norepinephrine
Potassium

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

@article{0092df68998947ed9c7462a6568d9fef,
title = "Effects of alpha adrenergic stimulations and blockade on early afterdepolarizations induced by cesium in canine cardiac Purkinje fibers",
abstract = "The effects of alpha adrenergic stimulation and three alpha adrenoceptor blockers on early afterdepolarizations (EADs) were examined in canine card diac Punkinje fibers. In the first group of 18 preparations, EADs were induced by superfusion with 7.5 mM cesium (Cs) dissolved in low potassium (2.7 mM KCI) Tyrode's solution. During alpha adrenoceptor stimulation (norepinephrine 1μM and propranolol 1μM) to enhance EADs, the effects of phentolamine and two new alpha 1 adrenoceptor antagonists, benoxathian and WB 4101 (1,3, and 10μM), were examined. WB 4101 (1μM) suppressed EADs in all six preparations. Benoxathian required 3μM in five preparations and 10 μM in one to suppress EADs. Phentolamine (10μM) suppressed EADs in two of six preparations. In the second group of 21 preparations, the effects on cesium-induced EADs of the three alpha adrenoceptor blockers (10μM) were examined without alpha adrenoceptor stimulation. WB 4101 (10μM) suppressed EADs in seven of seven preparations, while benoxathian (10μM) suppressed EADs in five of seven. Phentolamine (10μM) enhanced EADs in six of seven preparations. In the third group of 24 Purkinje fibers, the direct effects (without alpha adrenoceptor stimulation) of these three antagonists on the characteristics of normal Punkinje fiber action potentials superfused with normal Tyrode's solution were examined. Phentolamine (1,3, and 10μM, n = 8) prolonged action potential duration at 90{\%} repolarization (APD90) by 5.3{\%}±1.3{\%}, 10.0{\%} ± 1.8{\%}, and 14.3{\%} ± 2.7{\%}, respectively. Benoxathian (n = 8) and WB 4101 (n = 8) shortened APD90 equally: 6.8{\%} ± 1.1{\%} vs 7.7{\%} ± 1.3{\%} at 1 μM, 13.6{\%} ± 1.0{\%} vs 14.5{\%} ± 1.6{\%} at 3 μM, and 21.1{\%} ± 1.2{\%} vs 20.8{\%} ± 2.1{\%} at 10μM, respectively. We conclude that in cesium treated Purkinje fibers: (1) Alpha adrenoceptor stimulation enhanced EADs; (2) Phentolamine was least effective in suppressing EADs, probably because of a direct effect that prolonged APD90; and (3) Although benoxathian and WB 4101 had similar effects on APD90, WB 4101 was more effective in suppressing EADs at lower concentations than benoxathian.",
author = "S. Kaseda and Zipes, {D. P.}",
year = "1990",
language = "English",
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journal = "Journal of Cardiovascular Electrophysiology",
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T1 - Effects of alpha adrenergic stimulations and blockade on early afterdepolarizations induced by cesium in canine cardiac Purkinje fibers

AU - Kaseda, S.

AU - Zipes, D. P.

PY - 1990

Y1 - 1990

N2 - The effects of alpha adrenergic stimulation and three alpha adrenoceptor blockers on early afterdepolarizations (EADs) were examined in canine card diac Punkinje fibers. In the first group of 18 preparations, EADs were induced by superfusion with 7.5 mM cesium (Cs) dissolved in low potassium (2.7 mM KCI) Tyrode's solution. During alpha adrenoceptor stimulation (norepinephrine 1μM and propranolol 1μM) to enhance EADs, the effects of phentolamine and two new alpha 1 adrenoceptor antagonists, benoxathian and WB 4101 (1,3, and 10μM), were examined. WB 4101 (1μM) suppressed EADs in all six preparations. Benoxathian required 3μM in five preparations and 10 μM in one to suppress EADs. Phentolamine (10μM) suppressed EADs in two of six preparations. In the second group of 21 preparations, the effects on cesium-induced EADs of the three alpha adrenoceptor blockers (10μM) were examined without alpha adrenoceptor stimulation. WB 4101 (10μM) suppressed EADs in seven of seven preparations, while benoxathian (10μM) suppressed EADs in five of seven. Phentolamine (10μM) enhanced EADs in six of seven preparations. In the third group of 24 Purkinje fibers, the direct effects (without alpha adrenoceptor stimulation) of these three antagonists on the characteristics of normal Punkinje fiber action potentials superfused with normal Tyrode's solution were examined. Phentolamine (1,3, and 10μM, n = 8) prolonged action potential duration at 90% repolarization (APD90) by 5.3%±1.3%, 10.0% ± 1.8%, and 14.3% ± 2.7%, respectively. Benoxathian (n = 8) and WB 4101 (n = 8) shortened APD90 equally: 6.8% ± 1.1% vs 7.7% ± 1.3% at 1 μM, 13.6% ± 1.0% vs 14.5% ± 1.6% at 3 μM, and 21.1% ± 1.2% vs 20.8% ± 2.1% at 10μM, respectively. We conclude that in cesium treated Purkinje fibers: (1) Alpha adrenoceptor stimulation enhanced EADs; (2) Phentolamine was least effective in suppressing EADs, probably because of a direct effect that prolonged APD90; and (3) Although benoxathian and WB 4101 had similar effects on APD90, WB 4101 was more effective in suppressing EADs at lower concentations than benoxathian.

AB - The effects of alpha adrenergic stimulation and three alpha adrenoceptor blockers on early afterdepolarizations (EADs) were examined in canine card diac Punkinje fibers. In the first group of 18 preparations, EADs were induced by superfusion with 7.5 mM cesium (Cs) dissolved in low potassium (2.7 mM KCI) Tyrode's solution. During alpha adrenoceptor stimulation (norepinephrine 1μM and propranolol 1μM) to enhance EADs, the effects of phentolamine and two new alpha 1 adrenoceptor antagonists, benoxathian and WB 4101 (1,3, and 10μM), were examined. WB 4101 (1μM) suppressed EADs in all six preparations. Benoxathian required 3μM in five preparations and 10 μM in one to suppress EADs. Phentolamine (10μM) suppressed EADs in two of six preparations. In the second group of 21 preparations, the effects on cesium-induced EADs of the three alpha adrenoceptor blockers (10μM) were examined without alpha adrenoceptor stimulation. WB 4101 (10μM) suppressed EADs in seven of seven preparations, while benoxathian (10μM) suppressed EADs in five of seven. Phentolamine (10μM) enhanced EADs in six of seven preparations. In the third group of 24 Purkinje fibers, the direct effects (without alpha adrenoceptor stimulation) of these three antagonists on the characteristics of normal Punkinje fiber action potentials superfused with normal Tyrode's solution were examined. Phentolamine (1,3, and 10μM, n = 8) prolonged action potential duration at 90% repolarization (APD90) by 5.3%±1.3%, 10.0% ± 1.8%, and 14.3% ± 2.7%, respectively. Benoxathian (n = 8) and WB 4101 (n = 8) shortened APD90 equally: 6.8% ± 1.1% vs 7.7% ± 1.3% at 1 μM, 13.6% ± 1.0% vs 14.5% ± 1.6% at 3 μM, and 21.1% ± 1.2% vs 20.8% ± 2.1% at 10μM, respectively. We conclude that in cesium treated Purkinje fibers: (1) Alpha adrenoceptor stimulation enhanced EADs; (2) Phentolamine was least effective in suppressing EADs, probably because of a direct effect that prolonged APD90; and (3) Although benoxathian and WB 4101 had similar effects on APD90, WB 4101 was more effective in suppressing EADs at lower concentations than benoxathian.

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