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Hypoxic release of calcium from the sarcoplasmic reticulum of pulmonary artery smooth muscle.

Abstract
The hypoxic constriction of isolated pulmonary vessels is composed of an initial transient phase (phase 1) followed by a slowly developing increase in tone (phase 2). We investigated the roles of the endothelium and of intracellular Ca2+ stores in both preconstricted and unpreconstricted intrapulmonary rabbit arteries when challenged with hypoxia (PO2 16-21 Torr). Removing the endothelium did not affect phase 1, but phase 2 appeared as a steady plateau. Removing extracellular Ca2+ had essentially the same effect as removing the endothelium. Depletion of sarcoplasmic reticulum Ca2+ stores with caffeine and ryanodine abolished the hypoxic response. Omitting preconstriction reduced the amplitude of the hypoxic response but did not qualitatively affect any of the above responses. We conclude that hypoxia releases intracellular Ca2+ from ryanodine-sensitive stores by a mechanism intrinsic to pulmonary vascular smooth muscle without the need for Ca2+ influx across the plasmalemma or an endothelial factor. Our results also suggest that extracellular Ca2+ is required for the release of an endothelium-derived vasoconstrictor.
AuthorsM Dipp, P C Nye, A M Evans
JournalAmerican journal of physiology. Lung cellular and molecular physiology (Am J Physiol Lung Cell Mol Physiol) Vol. 281 Issue 2 Pg. L318-25 (Aug 2001) ISSN: 1040-0605 [Print] United States
PMID11435205 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Ryanodine
  • Caffeine
  • Calcium
Topics
  • Animals
  • Caffeine (pharmacology)
  • Calcium (metabolism)
  • Extracellular Space (metabolism)
  • Hypoxia (metabolism, physiopathology)
  • In Vitro Techniques
  • Intracellular Membranes (metabolism)
  • Male
  • Muscle, Smooth, Vascular (metabolism, pathology)
  • Osmolar Concentration
  • Pulmonary Artery (metabolism, physiopathology)
  • Rabbits
  • Ryanodine (pharmacology)
  • Sarcoplasmic Reticulum (metabolism)
  • Vasoconstriction (drug effects)

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