1993 Fiscal Year Final Research Report Summary
Roles of cerebral dopaminergic system in the osmotic regulation of ADH release
| Project/Area Number |
04670090
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
環境生理学(含体力医学･栄養生理学)
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| Research Institution | NIIGATA UNIVERSITY |
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Principal Investigator |
YAMAGUTI Ken'ichi Niigata University School of Medicine Assistant Professor, 医学部, 助手 (50108023)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUTI Ken'ichi Niigata University School of Medicine Assistant Professor (50108023)
YAMAGUTI Ken'ichi Niigata University School of Medicine Assistant Professor (50108023)
YAMAGUTI Ken'ichi Niigata University School of Medicine Assistant Professor (50108023)
YAMAGUTI Ken'ichi Niigata University School of Medicine Assistant Professor (50108023)
YAMAGUTI Ken'ichi Niigata University School of Medicine Assistant Professor (50108023)
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| Project Period (FY) |
1992 – 1993
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| Keywords | osmoreceptor / antidinretic hormone / dopaminergic neuron / anteroventral third ventricle region / paraventricular nucleus / arcuate nucleus / ventral tegmental area / prostaglandin |
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| Research Abstract |
1. Dopamine (DA) injections into the paraventricular hypothalamic nucleus(PVN) in conscious rats produced AVP secretion larger than that elicited by the intracerebroventricular (icv) injections, whereas those into the anteroventral third ventricular region (AV3V) did not affect the release. However, a DA antagonist given into AV3V almost completely abolished the ADH release in response to an osmotic stimulus. Its administration into the ventral tegmental area (VTA) also showed potency to attenuate the osmotic ADH secretion. However, the antagonist applied into the PVN was without effect. These results suggest that dopaminergic neurons may act to mediate osmotic stimulation of ADH release in the AV3V and the VTA regions. The inability of AV3V injection of DA to alter ADH secretion may be explained by the possibility that DA requirement had sufficiently been satisfied by the endogenous production when it was applied exogenously.
2. ADH secretion provoked by icy injections of prostaglandin
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(PG) was not inhibited by prior icv administrations of DA antagonists, and that caused by icv DA was not affected by the pretreatment with an inhibitor of PG biosynthesis. These results suggest that the AVP-secreting mechanisums activated by DA and PGs may be separated one another, despite the observation that both the substances may play facilitatory roles in the osmotic release of ADH.
3. Destruction of catecholaminergic neurons located in the arcuate hypothalamic nucleus (ARC) by local injections of 6-hydroxydopamine (6-OHDA) potentiated ADH release in response to an osmotic stimulus. The treatment with 6-OHDA decreased noradrenaline content of the hypothalamic tissue including the injection sites. Although reduction in DA content was not noted after the 6-OHDA treatment, those results suggest that the catecholaminergic neurons of the ARC containing the tuberohypophysial dopaminergic neurons may function to prevent the osmotically stimulated ADH release. Therefore, it seems that ADH secretion in the hyperosmotic state may receive not only facilitatory but also inhibitory regulation through catecholaminergic systems located in the circumventricular structures.
4. The possibility that the neural mechanisms responsible for the inhibitory role may exist in the hypothalamic tissue including the ARC was also suggested by an in vitro experiment using the hypothalamo-neurohypophysial explant. Less
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