J Physiol Society Meetings
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Physiol Vol 498, Issue Pt 2 pp 503-510
Copyright © 1997 by The Physiological Society
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Thompson, R J
Right arrow Articles by Nurse, C A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Thompson, R J
Right arrow Articles by Nurse, C A

Developmental loss of hypoxic chemosensitivity in rat adrenomedullary chromaffin cells.

 R J Thompson, A Jackson and C A Nurse

Department of Biology, McMaster University, Hamilton, Ontario, Canada.

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.




This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
J. Buttigieg, S. T. Brown, M. Lowe, M. Zhang, and C. A. Nurse
Functional mitochondria are required for O2 but not CO2 sensing in immortalized adrenomedullary chromaffin cells
Am J Physiol Cell Physiol, April 1, 2008; 294(4): C945 - C956.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
M. Kobayashi-Miura, K. Shioji, Y. Hoshino, H. Masutani, H. Nakamura, and J. Yodoi
Oxygen sensing and redox signaling: the role of thioredoxin in embryonic development and cardiac diseases
Am J Physiol Heart Circ Physiol, May 1, 2007; 292(5): H2040 - H2050.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Cell Physiol.Home page
A. J. Rico, J. Prieto-Lloret, C. Gonzalez, and R. Rigual
Hypoxia and acidosis increase the secretion of catecholamines in the neonatal rat adrenal medulla: an in vitro study
Am J Physiol Cell Physiol, December 1, 2005; 289(6): C1417 - C1425.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
J. Lopez-Barneo, R. del Toro, K. L. Levitsky, M. D. Chiara, and P. Ortega-Saenz
Regulation of oxygen sensing by ion channels
J Appl Physiol, March 1, 2004; 96(3): 1187 - 1195.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1997 The Physiological Society.