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Publication Detail
Measurements of intracellular Ca2+ in dissociated type I cells of the rabbit carotid body.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Biscoe TJ, Duchen MR, Eisner DA, O'Neill SC, Valdeolmillos M
  • Publication date:
    09/1989
  • Pagination:
    421, 434
  • Journal:
    J Physiol
  • Volume:
    416
  • Status:
    Published
  • Country:
    England
  • Print ISSN:
    0022-3751
  • Language:
    eng
  • Keywords:
    Animals, Benzofurans, Calcium, Carbachol, Carotid Body, Cyanides, Fluorescent Dyes, Fura-2, Hydrogen-Ion Concentration, In Vitro Techniques, Membrane Potentials, Potassium, Rabbits, Sodium
Abstract
1. The carotid body chemoreceptors are stimulated in situ by cyanide (CN-), which mimics the effect of hypoxia. We have shown that CN- increases a calcium-dependent potassium conductance (gK(Ca)) in single type I cells dissociated from the carotid body of the rabbit. We have now used the Ca2(+)-sensitive fluorophore, Fura-2, to measure intracellular Ca2+ directly in single type I cells. 2. CN- reversibly increased [Ca2+]i from approximately 90 nM to a mean of approximately 200 nM. Some of this Ca2+ originated from an intracellular store, which was depleted by exposure to Ca2(+)-free solutions. Prolonged application of CN- caused a sustained increase in [Ca2+]i, suggesting that CN- impairs the removal or sequestration of Ca2+. 3. pHi measured with the dye BCECF (2,7-bis(2-carboxyethyl)-5(and-6)-carboxyfluorescein) did not change consistently in response to CN-, although pHi changed predictably in response to both ammonium chloride and to acidification of the superfusate with CO2. 4. Potassium-induced depolarization (35 mM-K+) caused a large, cadmium-sensitive rise in [Ca2+]i. The K(+)-induced Ca2+ load was used to study the regulation of [Ca2+]i. 5. The clearance of a Ca2+ load was slowed either by removal of [Na+]o or by application of CN-. This shows that both a Na+-Ca2+ exchange and an energy-dependent process or processes contribute to the regulation of [Ca2+]i. 6. Carbachol (CCh, 10-100 microM), which also hyperpolarizes type I cells, caused a small transient rise in [Ca2+]i, indicating release from an exhaustible intracellular pool. The response to CN- was unaffected by prior or continued exposure to CCh, suggesting that the two stimuli operate by distinct mechanisms. 7. The increased gK(Ca) seen in type I cells in response to CN- thus reflects a change in cellular Ca2+ homeostasis. The rise in [Ca2+]i presumably underlies the documented increase in transmitter release from the carotid body in response to CN-. If chemotransduction is a consequence of the release of transmitters from the type I cell, the response of the carotid body to CN-, and possibly also to hypoxia, is thus a direct consequence of the energy dependence of Ca2+ homeostasis in the type I cell.
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