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 language | English (US) |
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Pages (from-to) | H376-H380 |
Journal | American Journal of Physiology - Heart and Circulatory Physiology |
Volume | 264 |
Issue number | 2 33-2 |
DOIs | |
State | Published - 1993 |
Keywords
- N(G)-monomethyl-L- arginine
- endothelium-derived contracting factor
- vasospasm
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)