2002 Fiscal Year Final Research Report Summary
The interaction between vasopressin and oxytocin neurons after central salt loading
| Project/Area Number |
13670068
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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 | Miyazaki Medical College |
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Principal Investigator |
KATO Kazuo Miyazaki Medical College, Physiology, Assistant, 医学部, 助手 (80284834)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Fos positive neurons / hypertonic saline / congestive heart failure model / intrinsic vasopressin / sodium nitroprusside / 内因性バゾプレッシン系 |
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| 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
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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
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