Effects of Temperature and Stimulating Agents on Carotid Body Cells

Eyzaguirre, C.; Baron, Margarita; Gallego, Roberto

doi:10.1007/978-3-642-66755-8_11

Cited by 7 publications

(8 citation statements)

References 6 publications

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“…This association of transmitter release and excitation of afferent nerve activity is common to a number of chemostimuli, and has contributed to the idea that the catecholamine-containing type I cells, which lie in synaptic contact with the afferent sinus nerve endings (McDonald & Mitchell, 1975), are the sites of detection and transduction of chemostimuli (see Fidone & Gonzalez, 1986, for review). ]Patch-clamp studies have revealed that type I carotid body cells contain an array of ion channel types (Lopez-Barneo, Lopez-Lopez, Urenfa & Gonzalez, 1988;Duchen, Caddy, Kirby, Patterson, Ponte & Biscoe, 1988;Hescheler, Delpiano, Acker & Pietruschka, 1989;Peers, 1990a;Peers & O'Donnell, 1990) and that chemostimuli such as hypoxia and extracellular acidity selectively inhibit K+ currents in these cells, although the specific type of K+ current has not always been fully characterized (Lopez-Barneo et al 1988;Hescheler et al 1989;Peers, 1990a, b;Peers & O'Donnell, 1990). Such findings are consistent with earlier observations that chemostimuli most commonly depolarize type I cells (Eyzaguirre, Baron & Gallego, 1977;Eyzaguirre, 1981;Fidone & GonzaElez, 1986), although it remains to be demonstrated whether K+ current suppression alone causes type I cell depolarization, and what role this effect may play in stimulus-induced transmitter release.…”

Section: Introductionsupporting

confidence: 81%

“…Increases in sinus nerve discharge caused by a variety of natural and chemical stimuli (including acidity) are also closely associated with release of transmitter substances from type I carotid body cells, particularly dopamine (Rigual et al 1984;Obeso et al 1987). Microelectrode recordings from type I cells, have shown variable changes in the responses of membrane potential to chemostimuli (presumably due to the unavoidable damage caused by impalement of these small cells) but one consistent observation is that extracellular acidity causes type I cell depolarization (Eyzaguirre et al 1977;Eyzaguirre, 1981). This finding is consistent with more recent patch-clamp experiments which have demonstrated that lowered pH.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of Ca(2+)‐activated K+ currents by intracellular acidosis in isolated type I cells of the neonatal rat carotid body.

Peers¹,

Green²

1991

The Journal of Physiology

103

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SUMMARY1. K+ and Ca2+ currents were recorded from enzymatically isolated type I cells of the neonatal rat carotid body, using the whole-cell configuration of the patch-clamp technique. The effects of intracellular acidosis, caused by bath application of anions of weak acids (propionate and acetate), were tested on these currents.2. Bath application of propionate or acetate (10 or 20 mM) caused reversible reductions in K' current amplitudes. These effects were maximal at low, positive test potentials where a shoulder in the current-voltage relationship occurs due to the activation of Ca2+-activated K+ currents.3. Time-course studies showed propionate to cause a rapid initial reduction of K+ currents which recovered partially during its continued application. Removal of propionate produced small, transient overshoots of K+ current amplitudes. In the absence of propionate or acetate, bath application of the Na+-H+ exchange inhibitor amiloride caused slowly developing inhibition of K+ current amplitudes.4. Changing extracellular pH from 7-4 to 8-0 increased K+ current amplitudes, but at this pHo propionate caused smaller reductions in K+ currents than at a pHo of 7-4.5. In the presence of 0-1 mM-Cd2 , or in high-Mg2 (6 mM), low-Ca2+ (01 mM) solutions, the residual, Ca2+-independent K+ currents were unaffected by 20 mMpropionate or acetate.6. Ca2± channel currents were also recorded, using 10 mM-Ba2' as the charge carrier. These sustained currents were completely abolished by 0-1 mM-Cd2+ and were enlarged in the presence of 5 JtM-Bay K 8644, suggesting that the currents passed through L-type Ca2+ channels.7. Ca2+ channel currents were not significantly affected by intracellular acidosis caused by bath application of 10 mM-propionate or acetate. They were also unaffected by a reduction of the extracellular pH from 7-4 to 7 0. 8. It is concluded that intracellular acidosis selectively inhibits Ca2+-activated K+ currents in type I carotid body cells. The possible significance of this effect on chemotransduction in the intact carotid body is discussed.MS 8945

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Section: Introductionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Inhibition of Ca(2+)‐activated K+ currents by intracellular acidosis in isolated type I cells of the neonatal rat carotid body.

Peers¹,

Green²

1991

The Journal of Physiology

103

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show abstract

“…Changes in R, also did not follow a consistent pattern (162,163). These results are similar to, but less pronounced than, those obtained with cyanide or ACh.…”

Section: Effects Of Temperature On Mp and R Of Glomussupporting

confidence: 68%

Arterial Chemoreceptors

Eyzaguirre¹,

Fitzgerald²,

Lahiri³

et al. 1983

Comprehensive Physiology

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“…Although changes in membrane potential of the type I cells were not observed by Baron & Eyzaguirre (1977) and Eyzaguirre, Baron & Gallego (1977) with changes in [K+]0, these results should be interpreted with caution, since the measured resting membrane potentials (19-8 + 0-4 mV) were much smaller than those found in a later study (52-56 mV) (Hayashida & Eyzaguirre, 1979). In this regard membrane potential did not change on application of acetylcholine in the study , whereas it was found to markedly depolarize type I cells in the study by Hayashida & Eyzaguirre (1979).…”

Section: Discussionmentioning

confidence: 96%