Source:http://linkedlifedata.com/resource/pubmed/id/14644754
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2004-3-5
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pubmed:abstractText |
In rats with streptozotocin-induced diabetes mellitus for 10-20 days, we showed that the abundance of the major medullary transport proteins involved in the urinary concentrating mechanism, urea transporter (UT-A1), aquaporin-2 (AQP2), and the Na+-K+-2Cl- cotransporter (NKCC2/BSC1), is increased, despite the ongoing osmotic diuresis. To test whether vasopressin is necessary for these diabetes mellitus-induced changes in UT-A1, AQP2, or NKCC2/BSC1, we studied Brattleboro rats because they lack vasopressin. Brattleboro rats were given vasopressin (2.4 microg/day via osmotic minipump) for 5 or 12 days. At 5 days, vasopressin increased AQP2 protein abundance but decreased UT-A1 abundance compared with untreated Brattleboro rats. At 12 days, vasopressin increased the abundance of both UT-A1 and AQP2 proteins but did not alter NKCC2/BSC1. Next, untreated Brattleboro rats were made diabetic for 10 days by injecting them with streptozotocin (40 mg/kg). Diabetes mellitus increased the abundance of AQP2 and NKCC2/BSC1 proteins, but UT-A1 protein abundance did not increase. Third, vasopressin-treated Brattleboro rats were made diabetic with streptozotocin for 10 days. In vasopressin-treated Brattleboro rats, diabetes mellitus increased UT-A1, AQP2, and NKCC2/BSC1 protein abundances. Vasopressin significantly increased UT-A1 phosphorylation in vasopressin-treated diabetic Brattleboro rats but not in the other groups of Brattleboro rats. We conclude that 1) administering vasopressin to Brattleboro rats for 12 days, but not for 5 days, increases UT-A1 protein abundance and 2) vasopressin is necessary for the increase in UT-A1 protein in diabetic rats but is not necessary for the increase in AQP2 or NKCC2 proteins.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Aqp2 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Aquaporin 2,
http://linkedlifedata.com/resource/pubmed/chemical/Aquaporin 6,
http://linkedlifedata.com/resource/pubmed/chemical/Aquaporins,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Transport Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Renal Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Chloride Symporters,
http://linkedlifedata.com/resource/pubmed/chemical/UT-A1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Vasopressins,
http://linkedlifedata.com/resource/pubmed/chemical/sodium-potassium chloride...
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1931-857X
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
286
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
F760-6
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pubmed:dateRevised |
2011-4-28
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pubmed:meshHeading |
pubmed-meshheading:14644754-Animals,
pubmed-meshheading:14644754-Aquaporin 2,
pubmed-meshheading:14644754-Aquaporin 6,
pubmed-meshheading:14644754-Aquaporins,
pubmed-meshheading:14644754-Diabetes Mellitus, Type 1,
pubmed-meshheading:14644754-Female,
pubmed-meshheading:14644754-Kidney Concentrating Ability,
pubmed-meshheading:14644754-Kidney Medulla,
pubmed-meshheading:14644754-Male,
pubmed-meshheading:14644754-Membrane Transport Proteins,
pubmed-meshheading:14644754-Phosphorylation,
pubmed-meshheading:14644754-Rats,
pubmed-meshheading:14644754-Rats, Brattleboro,
pubmed-meshheading:14644754-Rats, Sprague-Dawley,
pubmed-meshheading:14644754-Renal Agents,
pubmed-meshheading:14644754-Sodium-Potassium-Chloride Symporters,
pubmed-meshheading:14644754-Vasopressins
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pubmed:year |
2004
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pubmed:articleTitle |
Role of vasopressin in diabetes mellitus-induced changes in medullary transport proteins involved in urine concentration in Brattleboro rats.
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pubmed:affiliation |
Emory Univ. School of Medicine, Renal Division, WMRB Rm. 338, 1639 Pierce Drive NE, Atlanta, GA 30322, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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