Liu H W, Wang Y X, Crofton J T, Funyu T, Share L
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163, USA.
Brain Res. 1996 May 6;719(1-2):14-22. doi: 10.1016/0006-8993(96)00054-6.
Increased plasma osmolality results in increased central as well as peripheral release of vasopressin. Experiments were carried out to determine whether, in this circumstance, vasopressin can act centrally to modulate its peripheral release. Prior to the start of a thirty-min i.v. infusion of 2.5 M or 0.15 M NaCl, the rats were given an intracerebroventricular (i.c.v.) injection of a peptide V1/V2 vasopressin antagonist (2 micrograms), OPC-31260 (60 micrograms), a non-peptide V2 antagonist, or 1-desamino-8-D-arginine vasopressin (dDAVP, 5 ng), a V2 agonist. Experiments with the peptide antagonist were carried out in male and non-estrous female rats. Since there were no differences between males and females in the measured responses, experiments with the other two drugs were carried out only in males. Pretreatment with either the V1/V2 antagonist or the V2 antagonist enhanced the increase in plasma vasopressin levels in response to the hypertonic saline infusion by about 50% at the end of 30 min. dDAVP, on the other hand, had no effect. None of the i.c.v. drugs had an affect on either the pressor or bradycardic responses to hypertonic saline infusion. These observations suggest that vasopressin can act centrally in a negative feedback fashion to attenuate its own release into the peripheral circulation in response to increased plasma osmolality.
血浆渗透压升高会导致血管加压素在中枢和外周的释放均增加。开展了实验以确定在这种情况下血管加压素是否能在中枢发挥作用来调节其外周释放。在开始静脉输注2.5 M或0.15 M氯化钠30分钟之前，给大鼠进行脑室内（i.c.v.）注射一种肽类V1/V2血管加压素拮抗剂（2微克）、OPC-31260（60微克，一种非肽类V2拮抗剂）或1-去氨基-8-D-精氨酸血管加压素（dDAVP，5纳克，一种V2激动剂）。肽类拮抗剂的实验在雄性和非发情期雌性大鼠中进行。由于在所测反应中雄性和雌性之间没有差异，另外两种药物的实验仅在雄性大鼠中进行。用V1/V2拮抗剂或V2拮抗剂预处理后，在30分钟末，对高渗盐水输注的反应中血浆血管加压素水平的升高增强了约50%。另一方面，dDAVP没有影响。脑室内注射的这些药物对高渗盐水输注引起的升压或心动过缓反应均无影响。这些观察结果表明，血管加压素可通过负反馈方式在中枢发挥作用，以减弱其自身因血浆渗透压升高而向外周循环的释放。
