ObjectiveThe present study was undertaken to examine whether arginine vasopressin (AVP) relaxes primate coronary artery and to analyse the mechanisms of its action in reference to endothelial nitric oxide and AVP receptor subtype.MethodsIsometrical tension responses to AVP and desmopressin were recorded in isolated monkey coronary arteries.ResultsAVP (10−9to 10−7mol/l) induced a concentration-related relaxation; endothelium-denudation abolished the response. Treatment withNG-nitro-L-arginine, but not the D-enantiomer, abolished the endothelium-dependent relaxation, which was restored by L-arginine. Treatment with SR49059 and [Pmp1,Tyr(Me)2]-Arg8-vasopressin, selective inhibitors of V1receptor subtype, attenuated the relaxant response to AVP, whereas the relaxation induced by sodium nitroprusside was not affected by SR49059. Desmopressin, a V2receptor agonist, up to 10−8mol/l did not elicit relaxation.ConclusionsIt is concluded that AVP-induced monkey coronary arterial relaxation is mediated via nitric oxide synthesized from L-arginine in association with stimulation of V1receptor subtypes in the endothelium.