| Popis: |
The role of extracellular calcium entry through the voltage-operated calcium channels in response to hypoxia is controversial. Earlier observations (Eyzaguirre and Zapata 1965, Delpiano and Acker, 1989)are that upon removal or depletion of extracellular Ca2+ in vitro, the carotid chemosensory discharge increased during the first 20–40 min and then diminished. At this stage the responses to hypoxia and acetylcholine were also attenuated. More recently Shirahata and Fitzgerald (1991) reported that Ca2+removal in situ during hypoxia was promptly followed by a decrease in the chemosensory activity. Fidone et al.(1982) reported that incubation of carotid body in the Ca2+ free medium reduced dopamine release due to hypoxia. Working with freshly isolated glomus cells Biscoe and Duchen (1990), reported that removal of extracellular Ca2+ or use of calcium channel blocker did not prevent an increase in the intracellular Ca2+ due to hypoxia. Also, the effects of metabolic inhibitors on Ca2+ rise was not blocked by the foregoing procedures. Accordingly they concluded that the Ca2+ entry through the voltage-operated channels was not required for the hypoxic chemoreception. Besides, for the voltage-operated channels to participate in the hypoxic response, the cells needed to be depolarized first but there was no consistent depolarization. However, Sato et al. (1991) found evidence for Ca2+ increase in the glomus cells during hypoxia, thus Ca2+ controversy persisted. Previously we tested the effects of inorganic blockers of Ca2+ channel (Di Giulio et al. 1990) on carotid chemosensory activity and responses to hypoxia and found that Co2+stimulated chemosensory discharge and did not block the response to hypoxia. Recently we extended the study using the divalent cations Ni2+,Cd2+ and Mn2+ on the chemosensory discharges in the cat carotid body in vivo. |
