Faculty Collaboration Database

Endothelium-dependent response of human internal mammary artery to hypoxia. Am J Physiol 1993 Feb;264(2 Pt 2):H376-80

Date

02/01/1993

Pubmed ID

8447453

DOI

10.1152/ajpheart.1993.264.2.H376

Scopus ID

2-s2.0-0027460199 (requires institutional sign-in at Scopus site)   28 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 F1 alpha production (n = 22, P < 0.05). The endothelium-dependent contraction to hypoxia could be attenuated by indomethacin (n = 6, P < 0.05) or NG-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.

Author List

Pearson PJ, Lin PJ, Evora PR, Schaff HV

Author

Paul Joseph Pearson MD, PhD Chief, Professor in the Surgery department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

6-Ketoprostaglandin F1 alpha
Arginine
Endothelium, Vascular
Humans
Hypoxia
Indomethacin
Mammary Arteries
Norepinephrine
Vasoconstriction
Vasodilation
omega-N-Methylarginine