The Effect of Vagus Inhibition on the Output of Potassium From the Heart

Howell, W. H.; Duke, W. W.

doi:10.1152/ajplegacy.1908.21.1.51

Cited by 62 publications

(6 citation statements)

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“…One may suppose, for instance, that during the inhibitory conductance change for which some evidence has been presented, the permeability of the dendrites is a]tered to ions whose movement normally maintains or restores the resting potential (20). In this connection the earlier results of Howell and Duke (23) and Lehnartz (28) on the potassium-liberating action of vagus stimulation should be recalled. In addition to potassium there are indications that at least one other ion, chloride, is involved (6).…”

Section: Discussionmentioning

confidence: 99%

Synaptic Inhibition in an Isolated Nerve Cell

Kuffler

Eyzaguirre

1955

The Journal of General Physiology

264

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Following the preceding studies on the mechanisms of excitation in stretch receptor cells of crayfish, this investigation analyzes inhibitory activity in the synapses formed by two neurons. The cell body of the receptor neuron is located in the periphery and sends dendrites into a fine muscle strand. The dendrites receive innervation through an accessory nerve fiber which has now been established to be inhibitory. There exists a direct peripheral inhibitory control mechanism which can modulate the activity of the stretch receptor. The receptor cell which can be studied in isolation was stimulated by stretch deformation of its dendrites or by antidromic excitation and the effect of inhibitory impulses on its activity was analyzed. Recording was done mainly with intracellular leads inserted into the cell body. 1. Stimulation of the relatively slowly conducting inhibitory nerve fiber either decreases the afferent discharge rate or stops impulses altogether in stretched receptor cells. The inhibitory action is confined to the dendrites and acts on the generator mechanism which is set up by stretch deformation. By restricting depolarization of the dendrites above a certain level, inhibition prevents the generator potential from attaining the "firing level" of the cell. 2. The same inhibitory impulse may set up a postsynaptic polarization or a depolarization, depending on the resting potential level of the cell. The membrane potential at which the inhibitory synaptic potential reverses its polarity, the equilibrium level, may vary in different preparations. The inhibitory potentials increase as the resting potential is displaced in any direction from the inhibitory equilibrium. 3. The inhibitory potentials usually rise to a peak in about 2 msec. and decay in about 30 msec. After repetitive inhibitory stimulation a delayed secondary polarization phase has frequently been seen, prolonging the inhibitory action. Repetitive inhibitory excitation may also be followed by a period of facilitation. Some examples of "direct" excitation by the depolarizing action of inhibitory impulses are described. 4. The interaction between antidromic and inhibitory impulses was studied. The results support previous conclusions (a) that during stretch the dendrites provide a persisting "drive" for the more central portions of the receptor cell, and (b) that antidromic all-or-none impulses do not penetrate into the distal portions of stretch-depolarized dendrites. The "after-potentials" of antidromic impulses are modified by inhibition. 5. Evidence is presented that inhibitory synaptic activity increases the conductance of the dendrites. This effect may occur in the absence of inhibitory potential changes.

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Section: Discussionmentioning

confidence: 99%

Synaptic Inhibition in an Isolated Nerve Cell

Kuffler

Eyzaguirre

1955

The Journal of General Physiology

264

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“…Some direct evidence for a role of potassium ions in vagal inhibition has, however, long existed. Howell and Duke (20) found that potassium ions are liberated from perfused frog hearts during vagal inhibition. This observation has been confirmed by Lehnartz (23) in a significant short note.…”

Section: Discussionmentioning

confidence: 99%

Vagal and Sympathetic Effects on the Pacemaker Fibers in the Sinus Venosus of the Heart

Hutter

Trautwein

1956

The Journal of General Physiology

336

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1. Action potentials from sinus venosus and auricle fibers of spontaneously beating frog hearts have been recorded with intracellular electrodes. 2. Sinus fibers show a slow depolarization, the pacemaker potential, during diastole. The amplitude of this potential varies in different parts of the sinus. In some fibers the membrane potential falls by 11 to 15 mv. during diastole and the transition to the upstroke of the action potential is comparatively gradual. In other regions the depolarization develops more slowly and the action potential takes off more abruptly from a higher membrane potential. It is proposed that the fibers showing the largest fall in membrane potential during diastole are the pacemaker fibers of the heart, and that the rest of the preparation is excited by conduction. In auricle fibers the membrane potential is constant during diastole. 3. The maximum diastolic membrane potential and the overshoot of the action potential vary inversely with the amplitude of the pacemaker potential. The highest values were measured in auricle fibers. 4. Stimulation of vagi suppresses the pacemaker potentials. While the heart is arrested the membrane potential of the sinus fibers rises to a level above the maximum diastolic value reached in previous beats. In 28 experiments vagal stimulation increased the membrane potential from an average maximal diastolic value of 55 mv. to a "resting" level of 65.4 mv. The biggest vagal polarization was 23 mv. 5. In contrast to the sinus fibers vagal inhibition does not change the diastolic membrane potential of frog auricle fibers. 6. Vagal stimulation greatly accelerates the repolarization of the action potential and reduces its amplitude. These changes were seen both in the sinus and in auricle fibers stimulated by direct shocks during vagal arrest. 7. The conduction velocity in the sinus venosus of the tortoise is reduced by vagal stimulation. Block of conduction often occurs. 8. In the frog sinus venosus sympathetic stimulation increases the rate of rise of the pacemaker potential, accelerating the beat. The threshold remains unchanged. The rate of rise of the upstroke and the amplitude of the overshoot are increased. 9. The analogies between the vagal inhibition of the heart and the nervous inhibition of other preparations are discussed.

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“…It has long been known that application ofacetylcholine or stimulation ofthe vagus nerve may influence ion transport in the heart. Howell & Duke (1908) showed that vagal stimulation in an isolated frog heart liberates potassium ions into the perfusion solution; and Loewi (1921) discovered that excitation of the vagus nerve released a chemical which he called Vagusstoff. Later Dale (1937) demonstrated that Vagusstoff was acetylcholine, which when it was released from the vagus nerve produced a decrease in both heart rate and strength of contraction.…”

Section: Introductionmentioning

confidence: 99%

Are acetylcholine‐induced increases in 42K efflux mediated by intracellular cyclic GMP in turtle cardiac pace‐maker tissue?

Fleming¹,

Giles²,

Lederer³

1981

The Journal of Physiology

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SUMMARY1. 42K efflux has been measured from small strips of turtle sinus venosus tissue in order: (a) to characterize further the pharmacology of the acetylcholine response and (b) to test whether cyclic guanosine 3': 5'-monophosphoric acid (cyclic GMP) is the intracellular mediator of this response.2. The 42K wash-out curves show that the fractional escape rate (FER) of 42K efflux is nearly constant after 60-80 min, indicating that after this time period 42K FER is controlled by barrier-limited diffusion from a single intracellular compartment.3. The threshold of the dose-response relationship for the acetylcholine-induced increase in 42K FER is about 10-8 M and the Km is 2'75 x 10-7 in non-eserinized preparations.4. This acetylcholine response is completely blocked by atropine; but nicotinic blockers produce no detectable reduction of it. 5. Exogenous application of lipid-soluble analogues of cyclic GMP (dibutyryl or 8-bromo-cyclic GMP applied at 2-3 mm for 30 min) failed to mimic the acetylcholineinduced augmentation of 42K FER. 6. Experiments in which sodium nitroprusside (5 x 10-4 M for 30 min) was applied in order to stimulate the guanylate cyclase and hence produce a large, maintained increase in intracellular cyclic GMP failed to show a significant increase in 42K FER.7. When acetylcholine (10-6 M) was applied in the presence of O[Ca2+]o (in an attempt to inhibit the guanylate cyclase) there was no significant reduction in the acetylcholine-induced increases in 42K FER.8. Hence, these three indirect tests indicate that the muscarinic acetylcholineinduced increase in 42K FER in cardiac pace-maker tissue is unlikely to be mediated entirely by changes in the levels of intracellular cyclic GMP.

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The Effect of Vagus Inhibition on the Output of Potassium From the Heart

Cited by 62 publications

References 0 publications

Synaptic Inhibition in an Isolated Nerve Cell

Synaptic Inhibition in an Isolated Nerve Cell

Vagal and Sympathetic Effects on the Pacemaker Fibers in the Sinus Venosus of the Heart

Are acetylcholine‐induced increases in 42K efflux mediated by intracellular cyclic GMP in turtle cardiac pace‐maker tissue?

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