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

为阐明热应激刺激与血管紧张素Ⅱ调节对大鼠血管加压素分泌的交互作用，我们研究了内毒素血症对大鼠血管加压素分泌的影响及其机制。我们还研究了人体运动过程中加压素释放的机制，静脉注射脂多糖（IPS）诱导的内毒素血症可诱导大鼠加压素释放和饮水行为，而血浆渗透压和血浆体积无任何变化。脑室内（i. C.（五）氯沙坦给药提示脑血管紧张素II通过AT 1受体参与了内毒素诱导的系统性加压素分泌和口渴反应。我们比较了在分级循环运动方案中血浆加压素浓度和血浆渗透压之间的关系，雷拉蒂 ...更多信息 在静息状态下输注高渗盐水时出现痉挛。低强度运动（<60%最大摄氧量（VO_2max））抑制渗透性加压素分泌，高强度运动（> 60%VO_2max）促进渗透性加压素分泌。血压和心率随运动强度的增加而增加，食管温度、血浆乳酸浓度和血浆ACTH浓度在60%VO_2max以上时升高。这些反应在高渗盐水输注期间未发生。结果提示，低强度运动时加压素分泌减弱可能是由于血压升高所致，而高强度运动时加压素分泌增加可能是由于体温升高和/或应激诱导的CRH分泌所致。此外，我们的研究结果表明，渗透性加压素分泌并不刺激垂体前叶分泌ACTH。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