Sato M
Department of Physiology, Akita University School of Medicine, Japan.
Brain Res. 1994 Oct 31;662(1-2):251-4. doi: 10.1016/0006-8993(94)90820-6.
The characteristics underlying the response of cytosolic Ca2+ ([Ca2+]i) to hypercapnic acidosis in clusters of cultured glomus cells of the adult rabbit carotid body were evaluated using fura-2 microscopic fluorometry. Application of CO2 by bubbling through both superfusions of bicarbonate-buffered saline and HEPES-buffered saline produced a rapid and sustained increase in [Ca2+]i. The [Ca2+]i response increased correspondingly with a rise in concentrations of CO2 to 20% but at a point between 20 and 50% adapted to CO2 and it decreased its linear assent. The hypercapnic acidosis-induced increase of [Ca2+]i was diminished by removing external Ca2+. Also the [Ca2]i response was reduced in dose-dependent fashion by the addition of the voltage-gated Ca2+ channel blocker D600. An additional response of [Ca2+]i to acetate was also diminished by Ca2+ removal. These results suggest that the [Ca2+]i response to hypercapnic acidosis involves an influx of external Ca2+ through voltage-gated Ca2+ channels.
