1995 Fiscal Year Final Research Report Summary
The investigation of the mechanisms and the rapy of renal edema from the acpect of cell porality.
| Project/Area Number |
06671133
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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 |
Kidney internal medicine
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| Research Institution | Kumamoto University (1995)
Tokyo Medical and Dental University (1994) |
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Principal Investigator |
NONOGUCHI Hiroshi Kumamoto University, Internal Medicine, Associate Professor, 医学部・附属病院, 講師 (30218341)
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| Project Period (FY) |
1994 – 1995
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| Keywords | antidiuretic hormone / V_2 receptor / V_1a receptor / edema / inner medullary collecting duct / chronic renal failure / vasopressin (AVP) |
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| Research Abstract |
We investigated immunohistochemical localization of V2 vasopressin (antidiuretic hormone) receptor along the nephron using a specific polyclonal antibody. V2 receptor was present in some of thick ascending limbs and all of pricipal and inner medullary collecting duct (IMCD) cells. Not only basolateral but also luminal membrane was stained by the antibody in collecting ducts, especially in terminal IMCD.Therefore, to learn the functional role of luminal V2 receptor in terminal IMCD,we investigated the luminal effects of vasopressin on osmotic water permeability (Pf), urea permeability (Pu), and cAMP accumulation using isolated perfused rat terminal IMCD.Luminal vasopressin caused a small increase in cAMP accumulation, Pf and Pu in the absence of bath vasopressin. In contrast, luminal vasopressin inhibited Pf and Pu by 30-65% in the presence of bath vasopressin by decreasing cAMP accumulation via V1a or oxytocin receptors and by an unknown mechanism via V2 receptors in the luminal membrane of terminal IMCD.Therefore, luminal vasopressin acts as an diuretic hormone rather than antidiuretic hormone in terminal IMCD.
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