Source:http://linkedlifedata.com/resource/pubmed/id/16582576
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
|
pubmed:dateCreated |
2006-6-7
|
pubmed:abstractText |
The conventional protein kinase C isoenzyme beta (PKC-beta) is expressed in various structures of mouse kidney. To get insights into the function, PKC-beta knockout (-/-) and wild-type (+/+) mice were studied. Under basal conditions, PKC-beta-/- mice exhibited a higher systolic blood pressure (in awake mice), normal plasma concentrations of Na+ and K+, and normal plasma pH. Urine osmolality and 24-hour excretion of fluid, Na+, K+ and albumin were not different between genotypes, but urine pH was more alkaline in PKC-beta-/- mice. Inulin clearance experiments under anesthesia confirmed a higher systolic blood pressure and revealed normal glomerular filtration rate and fractional excretion of fluid, Na+ and K+ in PKC-beta-/- mice. The ability to restrict renal Na+ excretion in response to a low Na+ diet was unaltered in PKC-beta-/- mice. Chronic acid loading (NH4Cl) did not affect blood pH in PKC-beta+/+ mice, but induced a modest metabolic acidosis in PKC-beta-/- mice. In conclusion, first evidence is presented that (i) PKC-beta contributes to the regulation of arterial blood pressure, and (ii) PKC-beta is required for normal acid-base balance, which may relate to its expression and function in intercalated cells of the collecting duct.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Ammonium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Diuretics,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium, Dietary,
http://linkedlifedata.com/resource/pubmed/chemical/protein kinase C beta
|
pubmed:status |
MEDLINE
|
pubmed:issn |
1420-4096
|
pubmed:author | |
pubmed:copyrightInfo |
Copyright 2006 S. Karger AG, Basel.
|
pubmed:issnType |
Print
|
pubmed:volume |
29
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
36-42
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:16582576-Acidosis,
pubmed-meshheading:16582576-Alternative Splicing,
pubmed-meshheading:16582576-Ammonium Chloride,
pubmed-meshheading:16582576-Anesthesia,
pubmed-meshheading:16582576-Animals,
pubmed-meshheading:16582576-Blood Pressure,
pubmed-meshheading:16582576-Diuretics,
pubmed-meshheading:16582576-Kidney Tubules, Collecting,
pubmed-meshheading:16582576-Mice,
pubmed-meshheading:16582576-Mice, Knockout,
pubmed-meshheading:16582576-Protein Kinase C,
pubmed-meshheading:16582576-Sodium, Dietary,
pubmed-meshheading:16582576-Wakefulness
|
pubmed:year |
2006
|
pubmed:articleTitle |
Mice lacking protein kinase C beta present modest increases in systolic blood pressure and NH4Cl-induced metabolic acidosis.
|
pubmed:affiliation |
Institute of Pharmacology and Toxicology, University of Tübingen, Tübingen, Germany.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|