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O<INF>2</INF> availability modulates transmembrane Ca<SUP>2+</SUP> flux via second-messenger pathways in anoxia-tolerant hepatocytes
- Source :
- Journal of Applied Physiology; March 1997, Vol. 82 Issue: 3 p776-783, 8p
- Publication Year :
- 1997
-
Abstract
- O<INF>2</INF> availability modulates transmembrane Ca<SUP>2+</SUP> flux via second-messenger pathways in anoxia-tolerant hepatocytes. J. Appl. Physiol. 82(3): 776-783, 1997.Transmembrane Ca<SUP>2+</SUP>-flux was studied from single isolated turtle hepatocytes by using a noninvasive Ca<SUP>2+</SUP>-selective self-referencing microelectrode. Cells in Ca<SUP>2+</SUP>-reduced culture medium demonstrated a vanadate-and lanthanum-inhibitable Ca<SUP>2+</SUP>-efflux of 4 × 10<SUP>−17</SUP> mol Ca<SUP>2+</SUP> · μm<SUP>−2</SUP> · s<SUP>−1</SUP> continuously over 170 h. This flux diminished with 50 nM phorbol 12-myristate 13-acetate, a protein kinase C (PKC) activator, and was reinstated on PKC deactivation with sphingosine. Progressive hypoxia resulted in a reversible suppression of Ca<SUP>2+</SUP> efflux to 90% of normoxic controls with an apparent Michaelis constant for oxygen of 145 μM. PKC activation was critical in this suppression, as anaerobic administration of sphingosine caused a Ca<SUP>2+</SUP> influx and cell rupture. Hypoxia was also associated with an altered pattern of adenosine-mediated control over Ca<SUP>2+</SUP> efflux. Adenosine (100 μM) elevated Ca<SUP>2+</SUP> efflux twofold in normoxia, but neither adenosine nor the A<INF>1</INF>-purinoreceptor antagonist 8-phenyltheophylline altered the observed anaerobic suppression. Aerobic administration of 2-10 mM KCN failed to reproduce the anaerobic suppression; however, in conjunction with 10 mM iodoacetate, complete metabolic blockade caused a Ca<SUP>2+</SUP> influx and cell rupture. These observations suggest modulatory control by oxygen over transmembrane Ca<SUP>2+</SUP> efflux involving second-messenger systems in the hypoxic transition.
Details
- Language :
- English
- ISSN :
- 87507587 and 15221601
- Volume :
- 82
- Issue :
- 3
- Database :
- Supplemental Index
- Journal :
- Journal of Applied Physiology
- Publication Type :
- Periodical
- Accession number :
- ejs1221578