Influence of Hypoxia on Endothelium-Derived NO-Mediated Relaxation in Rat Carotid, Mesenteric and Iliac Arteries

Abstract

Individual vascular beds exhibit differences in vascular reactivity. The present study examined the influence of hypoxia on endothelium-dependent, especially nitric oxide (NO)-mediated, relaxation in the isolated rat common carotid, superior mesenteric and external iliac arteries. Hypoxia for 1 and 3 h had no effects on the relaxations caused by acetylcholine (ACh) and sodium nitroprusside (SNP) in common carotid and external iliac arteries. In addition, NO synthase inhibitor N^G-nitro-<smlcap>L</smlcap>-arginine (<smlcap>L</smlcap>-NA, 10 μmol/l)-resistant, endothelium-dependent relaxations by ACh were also unaffected by hypoxia in these arteries. On the other hand, ACh-induced relaxation in superior mesenteric arteries was significantly impaired by exposure to hypoxia, while this condition did not affect the relaxation induced by SNP or ACh in the presence of <smlcap>L</smlcap>-NA. This impairment was partially prevented by treatment with tempol (3 mmol/l), a superoxide scavenger. These findings demonstrate a marked heterogeneity in response to hypoxia in rat arteries. Briefly, acute hypoxia induces impairment of endothelium-derived NO-mediated relaxation through the decrease in its bioavailability in the superior mesenteric, but not in common carotid or external iliac, arteries. Furthermore, superoxide seems to be one causal factor responsible for the undesirable effect of hypoxia.