Szczepanska-Sadowska E, Sobocinska J, Kozłowski S
Department of Clinical and Applied Physiology, School of Medicine, Warsaw, Poland.
Peptides. 1987 Nov-Dec;8(6):1003-9. doi: 10.1016/0196-9781(87)90128-8.
To determine whether centrally released vasopressin influences thirst, observations of osmotic thirst threshold, osmotic load excretion and postloading restitution of plasma osmolality were made in dogs in control experiments and during infusion of AVP antagonists into the third ventricle. Significant elevation of osmotic thirst threshold was elicited by infusion of d(CH2)5AVP at a rate of 0.2-2.0 micrograms.min-1 and of d(Et2)AVP at a rate of 0.3 micrograms.min-1 (V1 antagonists, weak V2 agonists) as well as by administration of d(CH2)5[D-Ile2,Abu4]AVP at a rate of 0.4 micrograms.min-1 (potent V2 antagonist, weak V1 antagonist). Administration of d(CH2)5AVP at a rate of 2.0 micrograms.min-1 was associated with a significant suppression of the postloading water intake and osmotic load excretion and with a delay in restitution of plasma osmolality. These findings indicate that centrally released vasopressin may participate in the control of thirst.
为了确定中枢释放的血管加压素是否影响口渴感，在对照实验以及向第三脑室输注抗利尿激素（AVP）拮抗剂的过程中，对狗的渗透口渴阈值、渗透负荷排泄以及血浆渗透压负荷后恢复情况进行了观察。以0.2 - 2.0微克·分钟⁻¹的速率输注d(CH₂)₅AVP和以0.3微克·分钟⁻¹的速率输注d(Et₂)AVP（V1拮抗剂，弱V2激动剂）以及以0.4微克·分钟⁻¹的速率给予d(CH₂)₅[D - Ile₂,Abu₄]AVP（强效V2拮抗剂，弱V1拮抗剂），均可引起渗透口渴阈值显著升高。以2.0微克·分钟⁻¹的速率给予d(CH₂)₅AVP与负荷后水摄入量和渗透负荷排泄的显著抑制以及血浆渗透压恢复延迟有关。这些发现表明，中枢释放的血管加压素可能参与口渴的调控。
