Abstract: OBJECTIVE To investigate the role of gap junctions (GJ) and the GJ channel protein connexins (Cxs) in arginine vasopressin (AVP)-induced vasoconstriction after hemorrhagic shock. METHODS With a rat model of hemorrhagic-shock and hypoxia-treated vascular smooth muscle cells (VSMCs), the effects of GJ blockers carbenoxolone (CBX) and octanol, and the antisense oligodeoxynucleotides (AODNs) of Cxs on the AVP-mediated contractile response of superior mesenteric arteries (SMAs) after shock, and the effects of Cx37 and Cx43 on AVP-regulating the calcium sensitivity of SMAs after shock and intracellular calcium concentration in VSMCs after hypoxia were observed. RESULTS GJ blockers CBX and octanol significantly decreased the contractile response of SMAs to AVP after shock. Among all connexins that expressed in vessels, the AODNs of Cx37 and Cx43 significantly inhibited the vascular contractile effect of AVP after shock. Furthermore, Cx43AODN, but not Cx37AODN, significantly antagonized the AVP-induced increase of the calcium sensitivity of SMAs after shock. In addition, AVP treated or silencing of Cx37 and Cx43 had no significant influences on the intracellular calcium concentration in hypoxic VSMCs. CONCLUSION GJ plays an important role in AVP-mediated vascular contractile effect after hemorrhagic shock. Cx43 and Cx37 are the main isoforms of connexin involved. Cx43 plays effect mainly through AVP-mediated calcium sensitization pathway, while Cx37 may be through other mechanisms.