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. 1997 Jan 15;498(Pt 2):503–510. doi: 10.1113/jphysiol.1997.sp021876

Developmental loss of hypoxic chemosensitivity in rat adrenomedullary chromaffin cells.

R J Thompson 1, A Jackson 1, C A Nurse 1
PMCID: PMC1159219  PMID: 9032697

Abstract

1. We investigated whether adrenomedullary chromaffin cells (AMCs) derived from neonatal (postnatal day (P) 1-P2) and juvenile (P13-P20) rats, and maintained in short-term culture (1-3 days), express O2-chemoreceptive properties. 2. In whole-cell recordings, the majority (approximately 70%; n = 47) of neonatal AMCs were sensitive to hypoxia. Under voltage clamp, acute hypoxia (PO2 approximately 40 mmHg) suppressed voltage-dependent K+ current by 25.1 +/- 3.4% (mean +/- S.E.M.; n = 22); under current clamp, acute hypoxia caused a membrane depolarization of 14.1 +/- 1.3 mV (n = 13) from a resting potential of -54.8 +/- 2.8 mV (n = 13), and this was often sufficient to trigger action potentials. 3. Exposure of neonatal AMC cultures to a moderate (PO2 approximately 75 mmHg) or severe (PO2 approximately 35 mmHg) hypoxia for 1 h caused a dose-dependent stimulation (approximately 3 or 6 times normoxia, respectively) of catecholamine (CA) release, mainly adrenaline, determined by HPLC. This induced CA release was abolished by the L-type calcium channel blocker, nifedipine (10 microM). 4. In contrast to the above results in neonates, hypoxia had no significant effects on voltage-dependent K+ current, membrane potential, or CA release in juvenile AMCs. 5. We conclude that rat adrenal chromaffin cells possess a developmentally regulated O2-sensing mechanism, similar to carotid body type I cells.

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Selected References

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