Objective  To study the effect of hypoxia-inducible factor-1α (HIF-1α) on endothelium-dependent and -independent vascular relaxation reactivity following hemorrhagic shock in rats.   Methods  Two hundred and eight SD rats were randomly divided i

nto normal control group

shock control group and oligomycin group. Shock control and oligomycin groups were further divided into 0

0.5

1

2

3

and 4 h groups after hemorrhagic shock. Superior mesenteric artery (SMA) was used to compare the changes in vascular response to sodium nitroprusside (SNP) and acetylcholine (Ach) with or without administration of oligomycin

a kind of specific HIF-1α blocking agent

and to determine the expression of HIF-1α mRNA by RT-PCR.   Results  The vascular reactivity of SMA to SNP in each shock group was significantly decreased at lower concentrations (10

-9

10

-8

and 10

-7

mol/L) of SNP and oligomycin further depressed the response of SMA to SNP. The response of SMA to Ach in shock groups was transiently decreased after shock

and then began to increase during the compensatory period of shock

reached its peak at 2 h after shock

and then decreased again. The response of SMA to Ach decreased significantly in early hemorrhagic shock (0 to 1 h

P0.01) and increased in late hemorrhagic shock (2 to 4 h) after administration of oligomycin. HIF-1α mRNA expression increased in a timedependent manner and reached its peak at 4 h following shock

which was positively correlated with endothelium-dependent vascular relaxation reactivity in early hemorrhagic shock（r=0.984，P0.05）

negatively correlated with late hemorrhagic shock and did not correlate with endothelium-dependent vascular relaxation reactivity（r=-0.999，P0.05）.   Conclusion  Endothelium-dependent vascular relaxation reactivity increases in early hemorrhagic shock and decreases in late hemorrhagic shock. Endothelium-independent vascular relaxation reactivity decreases markedly following hemorrhagic shock. HIF-1α plays an important role in regulation of endothelium-dependent and independent vascular relaxation reactivity following hemorrhagic shock.