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Le résumé fourni par la source

Arginine vasopressin (AVP) produced relaxations at low concentrations (10-11and 10-10M)and contractions at higher concentrations in canine ciliary arterial strips with endothelium, partially contracted with prostglandin F2α. The AVP-induced relaxation was abolished or reversed to a contraction by removal of the endothelium or treatment with NG-nitro-L-arginine. The effect of this antagonist was reversed by L-arginine. The relaxant response was inhibited dose-dependently by SR49059 (10–10–10–9M), [Pmp1Tyr(Me)2]-Arg8-vasopressin (PMP-AVP) (10–10–10–9M), V1 receptor antagonists, and OPC31260 (3 × 10-8M), a reported V2 receptor antagonist, but not by OPC21268 (10–7–10–6M), a reported V1 antagonist. In the endothelium-denuded strips, the AVP-induced contraction was attenuated by SR49059, PMP-AVP and OPC31260, but not by OPC21268. It is concluded that AVP in low concentrations elicits intense relaxation of canine ciliary arteries, possibly due to nitric oxide synthesized in association with activation of the endothelial V1 receptor subtype. AVP-induced contractions appear to be mediated also by the V1 receptor in smooth muscle. Antagonistic selectivities of the OPC compounds to vasopressin receptor subtypes could not be seen in this particular material.

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