Interaction of stress defending system, thermoregulation and osmoregulation in the systemic vasopressin release

为了阐明热、应激刺激和渗透调节对全身加压素分泌的交互作用，我们研究了内毒素血症对大鼠加压素释放的影响及其机制。我们还研究了人类运动中加压素释放的机制。静脉注射脂多糖(IPS)引起的内毒素血症诱导了大鼠的加压素释放和摄水行为，而血浆渗透压和血浆容量没有任何变化。脑室内(I.C.V.)给予血管紧张素II AT1受体拮抗剂氯沙坦几乎完全抑制了这些反应，提示脑血管紧张素II通过AT1受体参与了内毒素诱导的全身加压素分泌和口渴。为了揭示人类运动中加压素释放的机制，我们比较了在分级循环ERGO运动方案中血浆加压素浓度与血浆渗透压的关系及其与…的关系在静息状态下高渗盐水输注时会有更多的反应。低强度运动(&lt；60%最大摄氧量(VO_2max))可减少渗透性加压素的分泌，而大强度(&gt；60%VO_2max)运动可增加渗透性加压素的分泌。血压和心率随运动强度的增加而增加，食道温度、血浆乳酸浓度和血浆ACTH浓度在60%VO2max以上升高。这些反应在高渗盐水输注过程中没有发生。结果提示，低强度运动时渗透性加压素分泌减少可能与血压升高有关，而高强度运动时渗透性加压素分泌增加可能与体温升高和/或应激诱导的CRH分泌有关，CRH可刺激加压素的分泌。此外，我们的结果表明，渗透性加压素的分泌不能刺激垂体前叶的ACTH分泌。较少

To elucidate the interactive effect of thermal and stress stimuli and osmoregulation on systemic vasopressin secretion, we examined the effect of endotoxemia on vasopressin release and its mechanism in rats. We also examined the mechanism of vasopressin release during exercise in humans.Endotoxemia, induced by intravenous lipopolysaccharide (IPS) administration, induced vasopressin release and water ingestion behavior in rats without any changes in plasma osmolality or plasma volume. Intracerebroventricular (i. c. v.) administration of losartan (angiotensin II AT1 receptor antagonist) almost completely inhibited these responses, suggesting that the brain angiotensin II is involved in the LPS-induced systemic vasopressin secretion and thirst via AT1 receptor.To reveal the mechanism of vasopressin release during exercise in humans, we compared the relationship between plasma vasopressin concentration and plasma osmolality during a graded cycle ergo meter exercise protocol and this relati … More onship during hyper tonic saline infusion at rest. Exercise at lower intensity (< 60 % maximal oxygen uptake (VO_2max)) attenuated osmotic vasopressin secretion, and exercise at higher intensity (> 60 % VO_2max) augmented osmotic vasopressin secretion. Blood pressure and heart rate increased with the increase in exercise intensity, and esophageal temperature, plasma lactate concentration, and plasma ACTH concentration increased above 60 % VO_2max. These responses did not occur during hyper tonic saline infusion. The results suggest that the attenuated osmotic vaspressin secretion at the lower exercise intensity might be due to the increased blood pressure, and that the augmented osmotic vasopressin secretion at the higher exercise intensity might be due to the increased body core temperature and/or stress-induced CRH secretion, CRH has been reported to stimulate vasopressin secretion in dogs. In addition, our results demonstrated that osmotic vasopressin secretion did not stimulate ACTH secretion from the anterior pituitary gland. Less