Toda M, Ayajiki K, Okamura T, Azuma I, Toda N
Department of Pharmacology, Shiga University of Medical Sciences, Seta, Ohtsu, Japan.
Eur J Pharmacol. 1998 Mar 5;344(2-3):197-201. doi: 10.1016/s0014-2999(97)01600-2.
In isolated dog posterior ciliary arteries contracted with prostaglandin F2alpha, desmopressin (10(-10) to 10(-8) M), a vasopressin V2 receptor agonist, produced a concentration-related relaxation, which was reversed to a contraction by removal of the endothelium. Desmopressin was approximately 1/100 as potent as arginine vasopressin. Treatment with NG-nitro-L-arginine, a nitric oxide (NO) synthase inhibitor, reversed the desmopressin-induced relaxation to a contraction and the addition of L-arginine restored the relaxation. SR49059 ((2S)1-[(2 R3S)-(5-chloro-3-(2-chlorophenyl)-1-(3,4-methoxybenzene-s ulfony)-3-hydroxy-2,3-dihydro-1H-indole-2-carbonyl]-pyrrolidine-2-car boxamide), a selective vasopressin V1 receptor antagonist, suppressed the relaxation. In endothelium-denuded arteries, desmopressin-induced contractions were also inhibited by SR49059. It is concluded that desmopressin, although much less potent than vasopressin, relaxes ciliary arteries via a mediation of NO synthesized from L-arginine in the endothelium. Vasopressin V1-receptor Subtypes appear to be involved in the desmopressin-induced relaxation and contraction.
在与前列腺素F2α收缩的离体犬睫状后动脉中，去氨加压素（10⁻¹⁰至10⁻⁸ M），一种血管加压素V2受体激动剂，产生浓度相关的舒张作用，去除内皮后该舒张作用转变为收缩。去氨加压素的效力约为精氨酸血管加压素的1/100。用一氧化氮（NO）合酶抑制剂NG-硝基-L-精氨酸处理可使去氨加压素诱导的舒张转变为收缩，添加L-精氨酸可恢复舒张。选择性血管加压素V1受体拮抗剂SR49059（(2S)1-[(2R3S)-(5-氯-3-(2-氯苯基)-1-(3,4-甲氧基苯磺酰基)-3-羟基-2,3-二氢-1H-吲哚-2-羰基]-吡咯烷-2-甲酰胺）可抑制舒张。在内皮剥脱的动脉中，SR49059也可抑制去氨加压素诱导的收缩。结论是，尽管去氨加压素的效力远低于血管加压素，但它通过内皮中由L-精氨酸合成的NO介导使睫状动脉舒张。血管加压素V1受体亚型似乎参与了去氨加压素诱导的舒张和收缩。
