title: Role of gap junctions in the contractile response to agonists in the mesenteric resistance artery of rats with acute hypoxia.
abstract: Hypoxic exposure results in the vascular dysfunction and reduction of vasomotor responses and thus disrupts or reduces blood flow in the resistance arteries. Connexin (Cx)-mediated gap junctional intercellular communication (GJIC) serves a critical role in the regulation of vasomotor tone and the synchronized contraction of arteries, however whether the adverse effect of hypoxia on vasomotor responses in vascular smooth muscle layer of resistance arteries is involved in changes in the GJIC and the expression of Cx43 and Cx45 remains to be elucidated. Pressure myography, whole-cell patch clamp and western blot analysis were used to investigate the differences in expression and function of gap junction (GJ) in the vascular smooth muscle cells (VSMCs) of the mesenteric resistance artery (MRA) from Sprague‑Dawley (SD) rats in normoxia and acute hypoxia groups. In the present study, whole‑cell patch clamp measurements demonstrated a signiﬁcant reduction in the membrane capacitance and conductance in the VSMCs of the MRAs in the acute hypoxia (5 min) group (n=13) compared with the normoxia group (n=13), which suggested that exposure to acute hypoxia of 5 min decreased the coupling of the GJ between the VSMCs of MRAs in SD rats. Pressure myographic analysis demonstrated that 0.1‑100 µM phenylephrine (PE)‑induced MRA vasoconstriction was less sensitive under the acute hypoxic condition (n=7) compared with the normoxia condition (n=9) following treatment with 100 µM 2‑aminoethoxydiphenyl borate for 20 min. Compared with SD rats under normoxia, the PE‑initiated vasoconstrictive frequency and amplitude under acute hypoxia for 20, 40 and 60 min in the MRAs of SD rats was markedly attenuated (n=7). The results of western blot analysis indicated that the expression levels of Cx43 and Cx45 in MRA under acute hypoxia (1 h) were lower compared with normoxia. Cx43‑and Cx45‑mediated GJs serve a signiﬁcant role in the regulation of the vasomotor function of MRA during hypoxia and may be essential for the adjustment of vasomotor tone in response to acute hypoxia.
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
authors.forename: Huan
authors.initials: H
authors.lastname: Liu
authors.affiliation: Department of Pathophysiology, Medical College of Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
authors.forename: Xin-Zhi
authors.initials: XZ
authors.lastname: Li
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
authors.forename: Min
authors.initials: M
authors.lastname: Peng
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
authors.forename: Wei
authors.initials: W
authors.lastname: Ji
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
authors.forename: Lei
authors.initials: L
authors.lastname: Zhao
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
authors.forename: Liang
authors.initials: L
authors.lastname: Zhang
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
authors.forename: Jun-Qiang
authors.initials: JQ
authors.lastname: Si
authors.affiliation: Department of Physiology, Medical College of Shihezi University, Shihezi, Xinjiang 832002, P.R. China.
authors.forename: Ke-Tao
authors.initials: KT
authors.lastname: Ma
mesh_terms: D000208:Acute Disease; D000818:Animals; D001896:Boron Compounds / Q000494:pharmacology; D002450:Cell Communication; D018031:Connexin 43 / Q000378:metabolism; D017630:Connexins / Q000378:metabolism; D005260:Female; D017629:Gap Junctions / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology*; D010656:Phenylephrine / Q000494:pharmacology; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D001896:Boron Compounds; D018031:Connexin 43; D017630:Connexins; D014662:Vasoconstrictor Agents; C082920:connexin 45; D010656:Phenylephrine; C109986:2-aminoethoxydiphenyl borate