Measurements of potassium changes in the cat carotid body under hypoxia and hypercapnia

Acker, H.; Dufau, E.; Sylvester, D.

doi:10.1007/bf00582434

Cited by 12 publications

(5 citation statements)

References 5 publications

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“…The hypothesis was originally proposed on the grounds that the membrane potential of all nerve cells is determined by ionic concentration gradients which are controlled by the sodium pump. A fall in oxygen tension would slow the pump, allowing a loss of potassium which in turn depolarizes the nerve endings and initiates action potentials in the afferent fibre; it has been shown that raising the extracellular potassium concentration increases chemoreceptor discharge (Jarisch, Landgren, Neil & Zotterman, 1952;Acker, 1978). The sodium pump is inhibited by ouabain (e.g.…”

Section: Discussionmentioning

confidence: 99%

Effects of ouabain on carotid body chemoreceptor activity in the cat.

McQueen¹,

Ribeiro²

1983

The Journal of Physiology

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SUMMARY1. The effects of infusions of ouabain on chemoreceptor activity recorded from the peripheral end of a sectioned carotid sinus nerve were studied in cats anaesthetized with pentobarbitone.2. Ouabain caused a marked increase in chemoreceptor discharge followed by a decline in discharge to frequencies near or below the pre-ouabain level; during the latter period further administration of ouabain had no effect.3. Infusion of ouabain during hypoxia further increased the chemoreceptor discharge, but this effect was short-lasting.4. On intracarotid administration ouabain was less effective in cats with the ganglioglomerular (sympathetic) nerves cut, whereas on intravenous administration no significant difference was observed. Following intravenous administration of ouabain the chemoreceptor peak discharge occurred with dose levels similar to those needed to cause cardiac arrhythmias, but following intracarotid administration the chemoreceptor discharge peaked at doses about 40 % of those causing arrhythmias.5. During ouabain-induced excitation the stimulatory action of NaCN, CO2-equilibrated Locke solution and acetylcholine was potentiated, as was the chemoinhibition induced by dopamine. During the post-excitatory period the responses evoked by these substances were reduced or abolished.6. Neither mecamylamine, a nicotinic antagonist, nor physostigmine, an anticholinesterase, affected the response of the carotid chemoreceptors to ouabain.7. The major finding of this study was that ouabain initially 'sensitizes' the carotid body chemoreceptors and then 'desensitizes' them. The most likely mechanism responsible for these effects is the well established Na+-K+-ATPase-inhibiting property of ouabain.

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Section: Discussionmentioning

confidence: 99%

Effects of ouabain on carotid body chemoreceptor activity in the cat.

McQueen¹,

Ribeiro²

1983

The Journal of Physiology

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“…The depolarizing property of potassium was first implicated in the mechanism of excitation of arterial chemoreceptors by Mills & Jobsis (1972), who hypothesized that in hypoxia a potassium pump might start to fail and allow potassium to build up in the confined extracellular space around the afferent nerve endings. Although Mills and Jobsis provided no direct evidence for the involvement of K+, Acker (1978) has since shown that its extracellular concentration in the carotid body is markedly increased in extreme hypoxia but not in hypercapnia.…”

Section: Introductionmentioning

confidence: 99%

Effects of potassium, oxygen and carbon dioxide on the steady‐state discharge of cat carotid body chemoreceptors.

Burger¹,

Estavillo²,

Kumar³

et al. 1988

The Journal of Physiology

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SUMMARY1. We have studied the effects of intravenous infusions of 0.1 mmol/min KCl (raising arterial potassium from ca. 3-2 to 6-0 mM) on the steady-state responses of carotid body chemoreceptors to end-tidal Pco2 and Po2 in the pentobarbitoneanaesthetized cat.2. The excitatory effect of these KCl infusions was enhanced by hypoxia and reduced or abolished by hyperoxia.3. Hypercapnia did not enhance, and usually reduced, excitation by KCl. 4. When similar control discharge frequencies were established by hypoxia or by hypercapnia, a KCl infusion excited the hypoxic discharge by about twice as much as it did the hypercapnic discharge.5. These observations are not inconsistent with the idea that the mechanism underlying hypoxic excitation of arterial chemoreceptors is one that controls extracellular potassium concentration near the afferent nerve ending.6. Insofar as potassium-induced excitation of chemoreceptor discharge is abruptly reduced by hyperoxia it behaves like Asmussen and Nielsen's postulated 'anaerobic work substance' and it may therefore contribute to the increased importance of the arterial chemoreflex reported in exercise.

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“…Frog skins were studied with single-barrelled microelectrodes drawn from (Acker, 1978;DeLong & Civan, 1979); when filled with 3 M KC1 solution and tested in Ringer's solution, such reference barrels had resistances as high as 100 M~. The singlebarrelled micropipettes had lower resistance (approximately 40 Mf~ under similar conditions), and were insensitive to the ionic strength of the ambient medium; such micropipettes were filled with 0.5 M KC1 solution in order to reduce the rate of release of KC1 into the cell during extended impalements (Nelson, Ehrenfeld & Lindemann, 1978).…”

Section: Methodsmentioning

confidence: 99%

Microelectrode study of K+ accumulation by tight epithelia: II. Effect of inhibiting transepithelial Na+ transport on reaccumulation following depletion

DeLong

Civan

1983

J. Membrain Biol.

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The effects of restoring serosal potassium to potassium-depleted toad urinary bladders have been re-examined using double-barrelled microelectrodes. The data confirm the existence of a time-lag phenomenon, a dissociation between potassium reaccumulation and restoration of short-circuit current. Returning serosal potassium stimulates an increase in intracellular potassium activity 21-26 min before any increase can be detected in short-circuit current. The reaccumulation of potassium has been further studied using split frog skin, a far more suitable preparation for electrophysiologic study than toad bladder. Under baseline short-circuited conditions, potassium is accumulated against an electrochemical gradient of 22 +/- 4 mV. Reaccumulation of potassium by potassium-depleted tissues can be blocked by inhibiting the Na,K-exchange pump with high concentrations of ouabain. On the other hand, blocking apical sodium entry by the addition of 10(-4) M amiloride to the outer bathing medium does not interfere with reaccumulation of potassium. The data support the concept that the time-lag phenomenon of toad bladder reflects stimulation of potassium reaccumulation by the sodium pump in exchange for the extrusion of excess cell sodium collected during the period of potassium depletion. This reaccumulation of potassium can proceed before the entry of significant added amounts of sodium across the apical plasma membrane.

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Measurements of potassium changes in the cat carotid body under hypoxia and hypercapnia

Cited by 12 publications

References 5 publications

Effects of ouabain on carotid body chemoreceptor activity in the cat.

Effects of ouabain on carotid body chemoreceptor activity in the cat.

Effects of potassium, oxygen and carbon dioxide on the steady‐state discharge of cat carotid body chemoreceptors.

Microelectrode study of K+ accumulation by tight epithelia: II. Effect of inhibiting transepithelial Na+ transport on reaccumulation following depletion

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