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INTERMITTENT HYPOXIA IN RATS INHIBITS ENDOTHELIUM‐DEPENDENT VASODILATION
Author(s) -
Youngblood Victoria Marie,
Kanagy Nancy L.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.960.14
Subject(s) - dilator , tiron , endocrinology , phenylephrine , medicine , acetylcholine , chemistry , vasodilation , superoxide , hypoxia (environmental) , nitric oxide , endothelium , intermittent hypoxia , oxygen , blood pressure , biochemistry , obstructive sleep apnea , organic chemistry , enzyme
Rats exposed to eucapnic intermittent hypoxia (E‐IH) to mimic sleep apnea have elevated mean arterial pressure (MAP) and increased vascular production of superoxide anion (O 2 − ). We hypothesized that increased arterial O 2 − in rats exposed to E‐IH quenches NO to inhibit acetylcholine‐induced (ACh) dilation. To test this hypothesis, aortas were dissected from rats exposed to E‐IH or air cycling (Sham) for 14 days. Aortic segments were suspended in tissue baths containing physiological saline solution in the presence of the superoxide dismutase mimetic, tiron (10 μM), the eNOS inhibitor, nitro‐L‐arginine (L‐NNA, 100 μM) or vehicle. Increasing concentrations of ACh were added to endothelium‐intact aortic rings constricted to 50% of maximal tension with phenylephrine. ACh‐induced dilation was diminished in E‐IH aortas compared to Sham (75.5±4.0 vs 97.1±1.5, p<0.05). L‐NNA diminished dilation in both groups but dilation in E‐IH arteries was still less than that in Sham arteries (16.06±7.7 vs. 41.5±11.4, p <0.05). Tiron treatment appeared to increase ACh‐induced dilation in E‐IH aortic segments but had no effect on dilation in Sham segments. Consistent with our hypothesis, E‐IH appears to cause endothelial dysfunction that may be caused in part by loss of a non‐NOS dilator and in part by increased O 2 − scavenging of NO.