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  • Title: Augmentation of calcium current by hypoxia in carotid body glomus cells.
    Author: Summers BA, Overholt JL, Prabhakar NR.
    Journal: Adv Exp Med Biol; 2000; 475():589-99. PubMed ID: 10849699.
    Abstract:
    Several lines of evidence indicate that transduction of the hypoxic stimulus at the carotid body involves an increase in cytosolic Ca2+ ([Ca2+]i) via activation of voltage-gated Ca2+ channels in the glomus cells. However, reported responses to hypoxia include either no effect on or inhibition of Ca2+ current in glomus cells. The apparent discrepancy between the effects of hypoxia on [Ca2+]i and Ca2+ channel activity prompted us to re-examine the effects of low oxygen on Ca2+ currents in glomus cells. Experiments were performed on freshly dissociated glomus cells from rabbit carotid bodies. Ca2+ channel activity was monitored using the whole-cell configuration of the patch clamp technique with Ba2+ as the charge carrier. Hypoxia (pO2 = 40 mmHg) augmented the Ca2+ current by 24% (at 0 mV). This augmentation was seen in a CO2/HCO3- but not in a HEPES buffered extracellular solution. However, when the extracellular pH (pHo) of a HEPES buffered solution is lowered from 7.4 to 7.0, then the Ca2+ current in glomus cells is augmented by hypoxia by 20%. Nisoldipine, an L-type Ca2+ channel blocker (2 microM), prevented augmentation of the Ca2+ current by hypoxia. On the other hand, an N- and P-type Ca2+ channel blocker (2 microM omega-conotoxin MVIIC) did not prevent the augmentation of the Ca2+ current by hypoxia. Protein kinase C (PKC) inhibitors, staurosporine (100 nM) and bisindolylmaleimide (2 microM), prevented augmentation by hypoxia. Okadaic acid (100 nM), an inhibitor of serine/threonine phosphatases also prevented augmentation of Ca2+ current by hypoxia; whereas, norokadaone, an inactive analog of okadaic acid, had no effect. These results suggest that hypoxia augments Ca2+ current through L-type Ca2+ channels via a PKC and/or phosphatase-sensitive pathways.
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