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Effects of sympathetic nerve stimulation on the sino‐atrial node of the guinea‐pig.
Author(s) -
Choate J K,
Edwards F R,
Hirst G D,
O'Shea J E
Publication year - 1993
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1993.sp019924
Subject(s) - stimulation , medicine , repolarization , tachycardia , diastolic depolarization , excitatory postsynaptic potential , depolarization , cardiology , membrane potential , heart rate , nifedipine , chemistry , sinoatrial node , electrophysiology , anesthesia , calcium , blood pressure , inhibitory postsynaptic potential , biochemistry
1. The effects of sympathetic nerve stimulation on the generation of pacemaker action potentials, recorded from the sino‐atrial node of the guinea‐pig, were determined by using intracellular recording techniques. 2. Trains of stimuli applied to the right stellate ganglion led to an increase in heart rate after a delay of a few seconds. During the initial phase of the tachycardia the rate of discharge of pacemaker action potentials increased and the rate of diastolic depolarization increased, but both the peak diastolic potential and the maximum rate of rise of the action potentials were reduced. During the later phase of the tachycardia the peak diastolic potential, the amplitude of the action potentials, the maximum rate of rise and the rate of repolarization of the action potentials were increased. 3. When membrane potential recordings were made from sino‐atrial node cells, in which beating had been abolished by adding the organic calcium antagonist nifedipine, sympathetic nerve stimulation initiated excitatory junction potentials (EJPs) which had time courses similar to those of the tachycardias recorded from beating preparations. 4. Although both the tachycardias produced by either sympathetic nerve stimulation or added noradrenaline were largely abolished by beta‐adrenoceptor antagonists, the membrane potential changes recorded during the responses to sympathetic nerve stimulation or added noradrenaline were different. Bath‐applied noradrenaline caused a tachycardia which was associated with an increase in the amplitudes of pacemaker action potentials, an increase in the peak diastolic potential and a shortening in the duration of pacemaker action potentials. 5. The addition of agents which cause the accumulation of cyclic AMP in the cytoplasm of the cells produced a tachycardia which was associated with a similar sequence of changes in the membrane potentials to those produced by added noradrenaline; again the membrane potential changes produced by these agents differed from those produced by sympathetic nerve stimulation. 6. The results are discussed in relation to the idea that neurally released noradrenaline activates a set of receptors which cause tachycardia by increasing inward current flow during diastole, whereas added noradrenaline activates a set of receptors that are linked to a cyclic AMP‐dependent pathway which modifies the properties of some of the voltage‐dependent channels involved in pacemaking activity.