Endothelium-dependent response of human internal mammary artery to hypoxia

P. J. Pearson, P. J. Lin, P. R.B. Evora, H. V. Schaff

Research output: Contribution to journalArticle

27 Scopus citations

Abstract

To study the effect of hypoxia on vascular tone in human internal mammary artery (IMA), segments of IMA were suspended in organ chambers and contracted with norepinephrine (at a dose producing 30% of maximal contraction). Exposure of IMA segments with endothelium to hypoxia (partial pressure of oxygen, 38 ± 4 mmHg) resulted in a transient relaxation (47 ± 6%) followed by constriction (177 ± 8%) (n = 14). IMA segments without endothelium exhibited a gradual decrease in tension that almost completely counteracted vasoconstriction. The initial transient endothelium-dependent relaxation could be blocked by indomethacin (10-6 M) and was associated with a 51% increase in 6-ketoprostaglandin F(1α) production (n = 22, P < 0.05). The endothelium-dependent contraction to hypoxia could be attenuated by indomethacin (n = 6, P < 0.05) or N(G)-monomethyl-L-arginine (10-5 M; n = 9, P < 0.05) and was completely blocked by combination of these agonists (n = 6, P < 0.05). These experiments indicate that on exposure to hypoxia, the human IMA exhibits an initial prostacyclin-mediated relaxation followed by contraction due to the production of a constrictor prostanoid in addition to the inhibition of basal production of endothelium-derived relaxing factor.

Original languageEnglish (US)
Pages (from-to)H376-H380
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume264
Issue number2 33-2
DOIs
StatePublished - 1993

Keywords

  • N(G)-monomethyl-L- arginine
  • endothelium-derived contracting factor
  • vasospasm

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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