Figure 2.

Vasodilatory responses to ACh and SNP of aortas and MAs. O-GlcNAc levels influenced ACh-induced relaxant responses during IH exposure in the (A-D) aorta and (I-L) MA. The vasodilatory responses of both (A and B) aortas and (I and J) MAs to ACh were significantly inhibited by AIH exposure, which was prevented by PugNAc. CIH impaired ACh-induced vasodilation of mesenteric rings, which was partly improved by (K and L) ST045849 but did not have a noticeable effect on the (C and D) aortas. SNP-induced relaxation was similar among all groups in the (E-H) aorta and (M-P) MA. Neither AIH nor CIH treatment altered SNP-induced relaxation of (F and H) aortas and (N and P) MAs. The groups were as follows: i) AOD, arterial rings treated with DMSO (vehicle) and 3-h normoxia exposure; ii) AOP, arterial rings treated with PugNAc and 3-h normoxia exposure; iii) AOS, arterial rings treated with ST045849 and 3-h normoxia exposure; iv) AID, arterial rings treated with DMSO and 3-h IH exposure; v) AIP, arterial rings treated with PugNAc and 3-h IH exposure; vi) AIS, arterial rings treated with ST045849 and 3-h IH exposure; vii) COD, arterial rings from control rats treated with DMSO; viii) COP, arterial rings from control rats treated with PugNAc; ix) COS, arterial rings from control rats treated with ST045849; x) CID, arterial rings from CIH rats treated with DMSO; xi) CIP, arterial rings from CIH rats treated with PugNAc; and xii) CIS, arterial rings from CIH rats treated with ST045849. Data are presented as the mean ± SD (n=5). *P<0.05. ACh, acetylcholine; SNP, sodium nitroprusside; O-GlcNAc, O-linked-β-N-acetylglucosamine; IH, intermittent hypoxia; CIH, chronic intermittent hypoxia; PE, phenylephrine; MA, mesenteric artery.