Hypoxic pulmonary vasoconstriction: cyclic adenosine diphosphate-ribose, smooth muscle Ca2+ stores and the endothelium

Anthony Mark Evans, M Dipp

Research output: Other contribution

47 Citations (Scopus)

Abstract

Hypoxic pulmonary vasoconstriction (HPV) is unique to pulmonary arteries, and supports ventilation/perfusion matching. However, in diseases such as emphysema, HPV can promote hypoxic pulmonary hypertension (HPH), which ultimately leads to right heart failure. Since it was first described, the mechanisms underpinning HPV have remained obscure, and current therapies for HPH are poor. Previous investigations have suggested that HPV may be mediated by processes intrinsic to the pulmonary artery smooth muscle, and by the release of a vasoconstrictor(s) from the endothelium. It was thought that oxygen-sensitive ion channels in the smooth muscle cell membrane triggered HPV, and it has been argued that the endothelium-derived vasoconstrictor is endothelin-1. However, these proposals remain controversial. This review discusses the regulation by hypoxia of cyclic adenosine diphosphate-ribose production and Call release from the sarcoplasmic reticulum in pulmonary artery smooth muscle. The role of these processes in triggering maintained HPV is then related to its subsequent progression due to vasoconstrictor(s) release from the endothelium. (C) 2002 Elsevier Science B.V. All rights reserved.

Original languageEnglish
Volume132
Publication statusPublished - 22 Aug 2002

Keywords

  • Ca2+, release
  • sarcoplasmic reticulum
  • cyclic-adenosine diphosphate-ribose
  • redox state
  • smooth muscle
  • endothelium
  • pulmonary artery
  • hypoxic pulmonary vasoconstriction
  • hypoxia
  • RAT PULMONARY
  • ADP-RIBOSE
  • INTRAPULMONARY ARTERIES
  • CALCIUM
  • RELEASE
  • CELLS
  • ANTAGONIST
  • INHIBITION
  • HYPERTENSION
  • CONTRACTION

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