Hypoxia is known to affect both endothelial cell adenine nucleotide metabolism and release of vasoactive substances, but the link between these is unknown. Since the release of these vasoactive substances may be in part mediated by an increase in [Ca2+]i we investigated the effects of metabolic inhibitors on [Ca2+]i in indo-1 loaded cultured rat aortic endothelial cells. Inhibition of oxidative phosphorylation (NaCN, 2 mM) or substrate deprivation alone (no glucose) caused little change in [Ca2+]i. In contrast, combined inhibition of oxidative phosphorylation and substrate deprivation (NaCN, no glucose) caused a significant increase in [Ca2+]i. [Ca2+]i rose similarly even when cells were studied in the absence of external Ca2+. The greatest increase in [Ca2+]i occurred in the absence of substrate and during exposure to an inhibitor of glycolysis (iodoacetate, 2 mM). These results suggest a lack of endogenous oxidative substrate and a critical dependence on glycolytic metabolism.

Agency
National Institute of Health (NIH)
Institute
National Institute on Aging (NIA)
Type
Intramural Research (Z01)
Project #
1Z01AG000263-03
Application #
3789783
Study Section
Project Start
Project End
Budget Start
Budget End
Support Year
3
Fiscal Year
1992
Total Cost
Indirect Cost
Name
National Institute on Aging
Department
Type
DUNS #
City
State
Country
United States
Zip Code