Effects of oxygen tension on energetics of cultured vascular smooth muscle.
Author
Summary, in English
Chronic hypoxia is a clinically important condition known to cause vascular abnormalities. To investigate the cellular mechanisms involved, we kept rings of a rat tail artery for 4 days in hypoxic culture (HC) or normoxic culture (NC) (PO(2) = 14 vs. 110 mmHg) and then measured contractility, oxygen consumption (JO(2)), and lactate production (J(lac)) in oxygenated medium. Compared with fresh rings, basal ATP turnover (J(ATP)) was decreased in HC, but not in NC, with a shift from oxidative toward glycolytic metabolism. JO(2) during mitochondrial uncoupling was reduced by HC but not by NC. Glycogen stores were increased 40-fold by HC and fourfold by NC. Maximum tension in response to norepinephrine and the JO(2) versus tension relationship (JO(2) vs. high K(+) elicited force) were unaffected by either HC or NC. Force transients in response to caffeine were increased in HC, whereas intracellular Ca(2+) wave activity during adrenergic stimulation was decreased. Protein synthesis rate was reduced by HC. The results show that long-term hypoxia depresses basal energy turnover, impairs mitochondrial capacity, and alters Ca(2+) homeostasis, but does not affect contractile energetics. These alterations may form a basis for vascular damage by chronic hypoxia.
Department/s
- Islet cell physiology
- Vascular Physiology
- Department of Clinical Sciences, Malmö
- Cellular Biomechanics
Publishing year
2002
Language
English
Pages
110-117
Publication/Series
American Journal of Physiology: Heart and Circulatory Physiology
Volume
283
Issue
1
Links
Document type
Journal article
Publisher
American Physiological Society
Topic
- Physiology
Keywords
- Oxygen Consumption
- Oxygen : pharmacology
- Oxygen : metabolism
- Norepinephrine : pharmacology
- Vascular : metabolism
- Smooth
- Muscle
- Vascular : drug effects
- Lactic Acid : metabolism
- Intracellular Fluid : metabolism
- In Vitro
- Glycogen : metabolism
- Glucose : metabolism
- Glucose : deficiency
- Female
- Energy Metabolism : physiology
- Tail : blood supply
- Vasoconstrictor Agents : pharmacology
- Vasoconstriction : physiology
- Uncoupling Agents : pharmacology
- Vasoconstriction : drug effects
- Proteins : biosynthesis
- Rats
- Support
- Non-U.S. Gov't
- Energy Metabolism : drug effects
- Cell Hypoxia : physiology
- Calcium Signaling : physiology
- Arteries : metabolism
- Arteries : drug effects
- Animal
Status
Published
Research group
- Islet cell physiology
- Vascular Physiology
- Cellular Biomechanics
ISBN/ISSN/Other
- ISSN: 1522-1539