Prostaglandins modulate arterial cholesteryl ester metabolism. Academic Article uri icon

Overview

MeSH

  • 6-Ketoprostaglandin F1 alpha
  • Alprostadil
  • Animals
  • Arachidonic Acid
  • Arachidonic Acids
  • Arteriosclerosis
  • Cholesterol
  • Cyclic AMP
  • Dinoprostone
  • Epoprostenol
  • Humans
  • Hydrolysis
  • Prostaglandins E

MeSH Major

  • Cholesterol Esters
  • Muscle, Smooth, Vascular
  • Prostaglandins

abstract

  • Cholesterol and cholesteryl esters (CE) are the two major classes of lipids which accumulate in arteries during human arteriosclerosis. Mechanisms responsible for this arterial lipid accretion remain to be fully elucidated. In recent years, we have suggested that prostaglandins may have an important role in the modulation of intracellular arterial CE metabolism through their interaction with cyclic nucleotides. This hypothesis was based on observations that arteriosclerotic arteries produce less prostaglandins, particularly prostacyclin, and have altered CE synthetic and hydrolytic activities as compared to uninvolved arteries. This review is a summary of our present knowledge concerning the role of eicosanoids and cyclic nucleotides in the modulation of enzyme activities responsible for arterial CE synthesis and hydrolysis.

publication date

  • 1984

has subject area

  • 6-Ketoprostaglandin F1 alpha
  • Alprostadil
  • Animals
  • Arachidonic Acid
  • Arachidonic Acids
  • Arteriosclerosis
  • Cholesterol
  • Cholesterol Esters
  • Cyclic AMP
  • Dinoprostone
  • Epoprostenol
  • Humans
  • Hydrolysis
  • Muscle, Smooth, Vascular
  • Prostaglandins
  • Prostaglandins E

Research

keywords

  • Journal Article

Identity

Language

  • eng

PubMed ID

  • 6098442

Additional Document Info

start page

  • 218

end page

  • 227

volume

  • 32

number

  • 4