2001 Fiscal Year Final Research Report Summary
Interaction of stress defending system, thermoregulation and osmoregulation in the systemic vasopressin release
| Project/Area Number |
12670065
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Environmental physiology (including Physical medicine and Nutritional physiology)
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| Research Institution | Kyoto Prefectural University of Medicine |
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Principal Investigator |
TAKAMATA Akira Department of Physiology, Kyoto Prefectural University of Medicine Instructor, 医学部, 助手 (00264755)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Tomoyuki Department of Physiology, Kyoto Prefectural University of Medicine Instructor, 医学部, 助手 (90305566)
ITOH Toshiyuki Department of Physiology, Kyoto Prefectural University of Medicine Associate Professor, 医学部, 助教授 (90168360)
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| Project Period (FY) |
2000 – 2001
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| Keywords | vasopressin / plasma osmolality / endotoxemia / brain angiotensin / AT1 receptor / exercise / stress / ACTH |
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| Research Abstract |
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
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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
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Research Products
(12 results)
