Effects of autonomic neurohumors on transmembrane potentials of atrial plateau fibers.
Isolated canine atrial plateau fibers were treated with acetylcholine or norepinephrine to note the effects on the transmembrane potential. Acetylcholine, 1.0 or 2.0 mug/ml, consistently reduced the slope of inherent phase 4 depolarization. Increases in maximum diastolic potential and rising velocity occurred along with a decrease in overshoot. The plateau phase disappeared. Pretreatment with atropine, 1.0 mug/ml, prevented these responses, and alone this drug had no discernible effect. Norepinephrine consistently increased the slope of phase 4 depolarization. Frequently plateau fibers generated action potentials by the normal pacemaker mechanism. "Arrhythmias" characterized by spontaneous excitations were induced in 92% of the norepinephrine experiments. Norepinephrine also enhanced the plateau phase of the action potential and decreased the rising velocity and overshoot. Racemic propranolol, 1.0 mug/ml, blocked all the above effects including arrhythmias. Dextropropranolol, 1.0 mug/ml, did not block effects produced by norepinephrine. Acetylcholine, applied to fibers under treatment with norepinephrine, reduced the slope of norepinephrine-induced phase 4 depolarization and terminated induced arrhythmias.
Effects of autonomic neurohumors on transmembrane potentials of atrial plateau fibers. Isolated canine atrial plateau fibers were treated with acetylcholine or norepinephrine to note the effects on the transmembrane potential. Acetylcholine, 1.0 or 2.0 mug/ml, consistently reduced the slope of inherent phase 4 depolarization. Increases in maximum diastolic potential and rising velocity occurred along with a decrease in overshoot. The plateau phase disappeared. Pretreatment with atropine, 1.0 mug/ml, prevented these responses, and alone this drug had no discernible effect. Norepinephrine consistently increased the slope of phase 4 depolarization. Frequently plateau fibers generated action potentials by the normal pacemaker mechanism. "Arrhythmias" characterized by spontaneous excitations were induced in 92% of the norepinephrine experiments. Norepinephrine also enhanced the plateau phase of the action potential and decreased the rising velocity and overshoot. Racemic propranolol, 1.0 mug/ml, blocked all the above effects including arrhythmias. Dextropropranolol, 1.0 mug/ml, did not block effects produced by norepinephrine. Acetylcholine, applied to fibers under treatment with norepinephrine, reduced the slope of norepinephrine-induced phase 4 depolarization and terminated induced arrhythmias.