{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,14]],"date-time":"2026-03-14T03:39:19Z","timestamp":1773459559750,"version":"3.50.1"},"reference-count":33,"publisher":"American Physiological Society","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2000,9,1]]},"abstract":"<jats:p>Previous studies have suggested that voltage-gated Ca<jats:sup>2+<\/jats:sup>influx in glomus cells plays a critical role in sensory transduction at the carotid body chemoreceptors. The purpose of the present study was to determine the effects of hypoxia on the Ca<jats:sup>2+<\/jats:sup>current in glomus cells and to elucidate the underlying mechanism(s). Experiments were performed on freshly dissociated glomus cells from rabbit carotid bodies. Ca<jats:sup>2+<\/jats:sup>current was monitored using the whole cell configuration of the patch-clamp technique, with Ba<jats:sup>2+<\/jats:sup>as the charge carrier. Hypoxia (pO<jats:sub>2<\/jats:sub>= 40 mmHg) augmented the Ca<jats:sup>2+<\/jats:sup>current by 24 \u00b1 3% ( n= 42, at 0 mV) in a voltage-independent manner. This effect was seen in a CO<jats:sub>2<\/jats:sub>\/HCO<jats:sub>3<\/jats:sub><jats:sup>\u2212<\/jats:sup>-, but not in a HEPES-buffered extracellular solution at pH 7.4 ( n= 6). When the pH of a HEPES-buffered extracellular solution was lowered from 7.4 to 7.0, hypoxia augmented the Ca<jats:sup>2+<\/jats:sup>current by 20 \u00b1 5% ( n= 4, at 0 mV). Nisoldipine, an L-type Ca<jats:sup>2+<\/jats:sup>channel blocker (2 \u03bcM, n = 6), prevented, whereas, \u03c9-conotoxin MVIIC (2 \u03bcM, n = 6), an inhibitor of N and P\/Q type Ca<jats:sup>2+<\/jats:sup>channels, did not prevent augmentation of the Ca<jats:sup>2+<\/jats:sup>current by hypoxia, implying that low oxygen affects L-type Ca<jats:sup>2+<\/jats:sup>channels in glomus cells. Protein kinase C (PKC) inhibitors, staurosporine (100 nM, n = 6) and bisindolylmaleimide (2 \u03bcM, n = 8, at 0 mV), prevented, whereas, a protein kinase A inhibitor (4 nM PKAi, n = 10) did not prevent the hypoxia-induced increase of the Ca<jats:sup>2+<\/jats:sup>current. Phorbol 12-myristate 13-acetate (PMA, 100 nM), a PKC activator, augmented the Ca<jats:sup>2+<\/jats:sup>current by 20 \u00b1 3% ( n = 8, at 0 mV). In glomus cells treated with PMA overnight (100 nM), hypoxia did not augment the Ca<jats:sup>2+<\/jats:sup>current (\u22123 + 4%, n = 5, at 0 mV). Immunocytochemical analysis revealed PKC\u03b4-like immunoreactivity in the cytosol of the glomus cells. Following hypoxia (6% O<jats:sub>2<\/jats:sub>for 5 min), PKC\u03b4-like immunoreactivity translocated to the plasma membrane in 87 \u00b1 3% of the cells, indicating PKC activation. These results demonstrate that hypoxia augments Ca<jats:sup>2+<\/jats:sup>current through L-type Ca<jats:sup>2+<\/jats:sup>channels via a PKC-sensitive mechanism.<\/jats:p>","DOI":"10.1152\/jn.2000.84.3.1636","type":"journal-article","created":{"date-parts":[[2017,12,21]],"date-time":"2017-12-21T14:00:42Z","timestamp":1513864842000},"page":"1636-1644","source":"Crossref","is-referenced-by-count":39,"title":["Augmentation of L-Type Calcium Current by Hypoxia in Rabbit Carotid Body Glomus Cells: Evidence for a PKC-Sensitive Pathway"],"prefix":"10.1152","volume":"84","author":[{"given":"Beth A.","family":"Summers","sequence":"first","affiliation":[{"name":"Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffrey L.","family":"Overholt","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, School of Medicine, Case Western 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