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

In English

Författare

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.

Publiceringsår

2002

Språk

Engelska

Sidor

110-117

Publikation/Tidskrift/Serie

American Journal of Physiology: Heart and Circulatory Physiology

Volym

283

Issue

1

Dokumenttyp

Artikel i tidskrift

Förlag

American Physiological Society

Ämne

  • Physiology

Nyckelord

  • 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

Forskningsgrupp

  • Islet cell physiology
  • Vascular Physiology
  • Cellular Biomechanics

ISBN/ISSN/Övrigt

  • ISSN: 1522-1539