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The interaction between vasopressin and oxytocin neurons after central salt loading

Research Project

Project/Area Number 13670068
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Environmental physiology (including Physical medicine and Nutritional physiology)
Research InstitutionMiyazaki Medical College

Principal Investigator

KATO Kazuo  Miyazaki Medical College, Physiology, Assistant, 医学部, 助手 (80284834)

Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2002: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2001: ¥800,000 (Direct Cost: ¥800,000)
KeywordsFos positive neurons / hypertonic saline / congestive heart failure model / intrinsic vasopressin / sodium nitroprusside / 内因性バゾプレッシン系 / バゾプレツシン産生ニューロン / オキシトシン産生ニューロン / 心不全ラットモデル / バゾプレッシン産生ニューロン
Research Abstract

The interaction between vasopressin and oxytocin neurons.
We examined the effect of central salt loading on the neuronal activity in both vasopressin (AVP) and oxytocin (OT) neurons using double labeling techniques of immunohistochemistry. After blocking the endogenous vasopressin with vasopressin V_1 receptors antagonist, the neuronal activity ratio, which was calculated by divided the number of Fos positive neurons with the number of AVP or OT neurons, increased in the paraventricular nucleus (PVN) of the hypothalamus. On the other hand, the ratio in the supraoptic nucleus (SON) was conversely decreased. This decreased neuronal activity in the SON was compatible with the decreased systemic OT levels. Endogenous vasopressin induced by central salt loading might facilitate the secretion of OT to the peripheral circulation.
The role of endogenous vasopressin was modulated in the heart failure models.
We made the congestive heart failure (CHF) model rats by ligating the left coronary artery … More and used them after more than three weeks recovery. Then, hypertonic saline (HS : 0.67 M) were administered centrally to two groups. One is pretreated with vasopressin V_1 receptors antagonist and the other is administered with HS only. We divided the PVN into four regions for evaluation, medial (PVM), lateral (PVL), dorsomedial cap (PVDC), and entire PVN (e-PVN). After blocking the endogenous vasopressin by vasopressin V_1 receptors antagonist, the neuronal activity in the PVDC was enhanced in the normal rats group, but conversely the facilitation was disappeared in the CHF group compared with each HS-administered alone group, respectively.
By what range does the pressor response during central salt loading become stress?
Previously, we showed that administration of high concentrated-HS (1.0 M) leveled off the neuronal activity in the PVN and SON. Then, we hypothesized that the greater pressor response might suppress the neuronal activity as previously reported. Although we tried to counter the pressor response during 1.0 M HS administration using sodium nitroprusside (SNP) from 26.5 ± 4.0 mmHg to -3.4 ± 3.8 mmHg, the neuronal activity in the PVN and SON changed more suppressed. It is suggested that to manipulate the blood pressure forcibly within normal range might become kind of stressor. Less

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • Research Products

    (10 results)

All Other

All Publications (10 results)

  • [Publications] Chu CP et al.: "Cardiovascular actions of central neuromedin U in conscious rats"Regul Pept. 105. 29-34 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Chu CP et al.: "Enhanced effects of central angiotensin II on cardiovascular and drinking responses in inbred polydipsic (STR/N) mince"Brain Res. 962. 129-134 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Jin QH et al.: "Possible involvement of nitric oxide in the central salt-loading-induced cardiovascular responses in conscious rats"Brain Res. 963. 224-231 (2003)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Chu CP, Jin QH, Kunitake T, Kato K, Nabekura T, Nakazato M, Kangawa K, Kannan H: "Cardiovascular actions of central neuromedin U in conscious rats"Regul Pept. 105. 29-34 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Chu CP, Kato K, Kunitake T, Watanabe S, Qiu DL, Ueta Y, Kannan H: "Enhanced effects of central angiotensin II on cardiovascular and drinking responses in inbred polydipsic (STR/N) mince"Brain Res. 962. 129-134 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Jin QH, Kunitake T, Chu CP, Qiu DL, Kato K, Ishizuka Y, Kannan H: "Possible involvement of nitric oxide in the central salt-loading-induced cardiovascular responses in conscious rats"Brain Res. 963. 224-231 (2003)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Chu C.-P.et al.: "Cardiovascular actions of central neuromedin U in conscious rats"Regul Pept. 105. 29-34 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Chu C.-P.et al.: "Enhanced effects of central angiotensin II on cardiovascular and drinking responses in inbred polydipsic (STR/N) mince"Brain Res. 962. 129-134 (2003)

    • Related Report
      2002 Annual Research Report
  • [Publications] Jun Q.-H.et al.: "Possible involvement of nitric oxide in the central salt-loading-induced cardiovascular responses in conscious rats"Brain Res. 963. 224-231 (2003)

    • Related Report
      2002 Annual Research Report
  • [Publications] Shirasaka T. et al.: "Orexin depolarizes rat hypothalamic paraventricular nucleus neurons"Am J Physiol. 281. R1114-R1118 (2001)

    • Related Report
      2001 Annual Research Report

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Published: 2001-04-01   Modified: 2016-04-21  

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