Desmopressin-induced dog ciliary artery relaxation.
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.[1]References
- Desmopressin-induced dog ciliary artery relaxation. Toda, M., Ayajiki, K., Okamura, T., Azuma, I., Toda, N. Eur. J. Pharmacol. (1998) [Pubmed]
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