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Effects of oxygen tension on energetics of cultured vascular smooth muscle.

Lindqvist, Anders LU ; Dreja, Karl LU ; Swärd, Karl LU and Hellstrand, Per LU (2002) In American Journal of Physiology: Heart and Circulatory Physiology 283(1). p.110-117
Abstract
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... (More)
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. (Less)
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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
in
American Journal of Physiology: Heart and Circulatory Physiology
volume
283
issue
1
pages
110 - 117
publisher
American Physiological Society
external identifiers
  • wos:000176156400015
  • pmid:12063281
  • scopus:0036299754
ISSN
1522-1539
DOI
10.1152/ajpheart.00040.2001
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Islet cell physiology (013212142), Vascular Physiology (013212034), Cellular Biomechanics (013212075), Unit on Vascular Diabetic Complications (013241510)
id
64b453b6-2d0c-4bcc-a394-6be19bb77665 (old id 108813)
alternative location
http://ajpheart.physiology.org/cgi/content/full/283/1/H110
date added to LUP
2016-04-01 12:19:28
date last changed
2022-01-27 02:01:48
@article{64b453b6-2d0c-4bcc-a394-6be19bb77665,
  abstract     = {{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.}},
  author       = {{Lindqvist, Anders and Dreja, Karl and Swärd, Karl and Hellstrand, Per}},
  issn         = {{1522-1539}},
  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}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{110--117}},
  publisher    = {{American Physiological Society}},
  series       = {{American Journal of Physiology: Heart and Circulatory Physiology}},
  title        = {{Effects of oxygen tension on energetics of cultured vascular smooth muscle.}},
  url          = {{http://dx.doi.org/10.1152/ajpheart.00040.2001}},
  doi          = {{10.1152/ajpheart.00040.2001}},
  volume       = {{283}},
  year         = {{2002}},
}