Hamu Y, Kanmura Y, Tsuneyoshi I, Yoshimura N
Department of Anesthesiology and Critical Care Medicine, Kagoshima University School of Medicine, Sakuragaoka, Japan.
Anesth Analg. 1999 Mar;88(3):542-8. doi: 10.1097/00000539-199903000-00015.
We studied the effects of vasopressin on contraction in normal and endotoxin-treated human gastroepiploic arterial rings in vitro. In this tissue, vasopressin (50-500 pg/mL) produced concentration-dependent, endothelium-independent contractions. Vasopressin also potentiated the contraction elicited by 1.0 micromol/L norepinephrine (NE) in both the presence and absence of endothelium. Endotoxin (10 microg/mL) attenuated the 1.0 micromol/L NE-induced contractions, and this attenuation was reversed by 300 micromol/L N(G)-nitro-L-arginine-methyl ester (L-NAME) and by 300 micromol/L N(G)-nitro-L-arginine (L-NoArg). After 12 h endotoxin treatment, the vasopressin-induced contraction was attenuated, and the enhancing effect of vasopressin was diminished. However, both before and after endotoxin, the enhancement produced by vasopressin was larger than the vasopressin-contraction itself. An antagonist of the vasopressin V1 receptor, 1.0 micromol/L beta-mercapto-[beta,beta-cyclopentamethylenpropionyl1,O-MeTyr2+ ++,Arg8]-vasopressin, and an antagonist of V1 + V2 receptor receptor, 1.0 micromol/L des-Gly9-[beta-mercapto-beta,beta-cyclopentamethylenepropionyl1 ,O-Et-Tyr2,Val,Arg8]-vasopressin, each diminished the vasopressin-induced enhancement of the NE contraction.
The results of our study suggest that, in addition to its direct vasoconstrictor effect, vasopressin strongly enhances the responses to norepinephrine through V1-receptor stimulation and that vasopressin could find a role in the management of endotoxin-induced vasodilation.
我们在体外研究了血管加压素对正常及内毒素处理的人胃网膜动脉环收缩的影响。在该组织中，血管加压素（50 - 500 pg/mL）产生浓度依赖性、不依赖内皮的收缩。在有内皮和无内皮的情况下，血管加压素还增强了1.0 μmol/L去甲肾上腺素（NE）引起的收缩。内毒素（10 μg/mL）减弱了1.0 μmol/L NE诱导的收缩，而300 μmol/L N(G)-硝基-L-精氨酸甲酯（L-NAME）和300 μmol/L N(G)-硝基-L-精氨酸（L-NoArg）可逆转这种减弱。内毒素处理12小时后，血管加压素诱导的收缩减弱，且血管加压素的增强作用减弱。然而，在内毒素处理前后，血管加压素产生的增强作用均大于其自身的收缩作用。血管加压素V1受体拮抗剂1.0 μmol/L β-巯基-[β,β-环五亚甲基丙酰基1,O-甲基酪氨酰2,精氨酰8]-血管加压素和V1 + V2受体拮抗剂1.0 μmol/L去甘氨酰-[β-巯基-β,β-环五亚甲基丙酰基1,O-乙基酪氨酰2,缬氨酰,精氨酰8]-血管加压素均减弱了血管加压素诱导的NE收缩增强作用。
我们的研究结果表明，除了其直接的血管收缩作用外，血管加压素通过刺激V1受体强烈增强对去甲肾上腺素的反应，并且血管加压素可能在内毒素诱导的血管舒张管理中发挥作用。
