Statements in which the resource exists as a subject.
PredicateObject
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
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: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