Am J Physiol Cell Physiol AJP: Gastrointestinal and Liver Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 274: C1592-C1600, 1998;
0363-6143/98 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Kumar, G. K.
Right arrow Articles by Prabhakar, N. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kumar, G. K.
Right arrow Articles by Prabhakar, N. R.
Vol. 274, Issue 6, C1592-C1600, June 1998

Release of dopamine and norepinephrine by hypoxia from PC-12 cells

Ganesh K. Kumar1, Jeffrey L. Overholt2, Gary R. Bright3, Kwong Y. Hui4, Hongwen Lu2, Miklos Gratzl4, and Nanduri R. Prabhakar2

Departments of 1 Biochemistry, 2 Physiology and Biophysics, 3 Anatomy, and 4 Biomedical Engineering, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106

We examined the effects of hypoxia on the release of dopamine (DA) and norepinephrine (NE) from rat pheochromocytoma 12 (PC-12) cells and assessed the involvement of Ca2+ and protein kinases in stimulus-secretion coupling. Catecholamine release was monitored by microvoltammetry using a carbon fiber electrode as well as by HPLC coupled with electrochemical detection (ECD). Microvoltammetric analysis showed that hypoxia-induced catecholamine secretion (PO2 of medium ~40 mmHg) occurred within 1 min after the onset of the stimulus and reached a plateau between 10 and 15 min. HPLC-ECD analysis revealed that, at any level of PO2, the release of NE was greater than the release of DA. In contrast, in response to K+ (80 mM), DA release was ~11-fold greater than NE release. The magnitude of hypoxia-induced NE and DA releases depended on the passage, source, and culture conditions of the PC-12 cells. Omission of extracellular Ca2+ or addition of voltage-gated Ca2+ channel blockers attenuated hypoxia-induced release of both DA and NE to a similar extent. Protein kinase inhibitors, staurosporine (200 nM) and bisindolylmaleimide I (2 µM), on the other hand, attenuated hypoxia-induced NE release more than DA release. However, protein kinase inhibitors had no significant effect on K+-induced NE and DA releases. These results demonstrate that hypoxia releases catecholamines from PC-12 cells and that, for a given change in PO2, NE release is greater than DA release. It is suggested that protein kinases are involved in the enhanced release of NE during hypoxia.

transmitter release; protein kinase; stimulus-secretion coupling


This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
D.-K. Kim, N. Natarajan, N. R. Prabhakar, and G. K. Kumar
Facilitation of dopamine and acetylcholine release by intermittent hypoxia in PC12 cells: involvement of calcium and reactive oxygen species
J Appl Physiol, March 1, 2004; 96(3): 1206 - 1215.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
D.-K. Kim, N. R. Prabhakar, and G. K. Kumar
Acetylcholine release from the carotid body by hypoxia: evidence for the involvement of autoinhibitory receptors
J Appl Physiol, January 1, 2004; 96(1): 376 - 383.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
G. K. Kumar, D.-K. Kim, M.-S. Lee, R. Ramachandran, and N. R. Prabhakar
Activation of tyrosine hydroxylase by intermittent hypoxia: involvement of serine phosphorylation
J Appl Physiol, August 1, 2003; 95(2): 536 - 544.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
D. R. D. Premkumar, R. R. Mishra, J. L. Overholt, M. S. Simonson, N. S. Cherniack, and N. R. Prabhakar
L-type Ca2+ channel activation regulates induction of c-fos transcription by hypoxia
J Appl Physiol, May 1, 2000; 88(5): 1898 - 1906.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
P. W. Conrad, T. L. Freeman, D. Beitner-Johnson, and D. E. Millhorn
EPAS1 trans-Activation during Hypoxia Requires p42/p44 MAPK
J. Biol. Chem., November 19, 1999; 274(47): 33709 - 33713.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
S. C. Taylor, T. F. C. Batten, and C. Peers
Hypoxic Enhancement of Quantal Catecholamine Secretion. EVIDENCE FOR THE INVOLVEMENT OF AMYLOID beta -PEPTIDES
J. Biol. Chem., October 29, 1999; 274(44): 31217 - 31222.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
P. W. Conrad, R. T. Rust, J. Han, D. E. Millhorn, and D. Beitner-Johnson
Selective Activation of p38alpha and p38gamma by Hypoxia. ROLE IN REGULATION OF CYCLIN D1 BY HYPOXIA IN PC12 CELLS
J. Biol. Chem., August 13, 1999; 274(33): 23570 - 23576.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
C. Smith
A Persistent Activity-Dependent Facilitation in Chromaffin Cells Is Caused by Ca2+ Activation of Protein Kinase C
J. Neurosci., January 15, 1999; 19(2): 589 - 598.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online