Premium
Prenatal anemia and adult coronary endothelial function
Author(s) -
Yang Qin,
Hohimer Roger A.,
Giraud George D.,
Winkle Donna M.Van,
Yim Anthony PC,
He GuoWei,
Davis Lowell E.
Publication year - 2007
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.21.6.a1382-c
Subject(s) - medicine , vasodilation , anemia , in utero , bradykinin , endocrinology , endothelial dysfunction , nitric oxide , cardiology , fetus , pregnancy , biology , genetics , receptor
We previously demonstrated cardiovascular adaptations to chronic fetal anemia with persistence into adult life. We further investigated whether the increase in coronary blood flow and in coronary conductance is attributable to augmented coronary endothelial function. Right coronary small arteries (diameter 200–450 μm) from 7‐month old adult sheep with in‐utero anemia were studied. The vasorelaxant response to bradykinin (BK, −10~−6.5 logM) was determined with the role of PGI 2 , nitric oxide (NO) and non‐NO‐non‐PGI 2 (NNONPG)‐mechanism explored. BK‐induced, endothelium‐dependent relaxation did not differ between the adult experienced in‐utero anemia (96.0±2.6%) and their non‐anemic siblings (control, 98.8±1.0%). Indomethacin did not affect the response to BK. Inhibition of NO markedly reduced the relaxation (repeated measures) in both anemic ( p <0.05) and control groups ( p <0.001) with EC 50 right shifted (anemia: −8.70±0.11 vs. −8.14±0.18 logM, p <0.05; control: −8.49±0.12 vs. −7.86±0.13 logM, p <0.01). The NNONPG‐mechanism contributed more in anemic animals ( p =0.022, two‐way ANOVA). Thus, both NO and NNONPG‐mechanisms, but unlikely the PGI 2 ‐mechanism are involved in sheep coronary vasodilatation. The NNONPG‐mechanism is slightly upregulated by in‐utero anemia although the endothelial function, as a whole, remains unchanged.