Linked Life Data

6755050

Source:http://linkedlifedata.com/resource/pubmed/id/6755050

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
19
pubmed:dateCreated
1983-1-19
pubmed:abstractText
Fractional chloride reabsorption in the thick ascending limb of the loop of Henle, measured by clearance techniques, is subnormal in patients with Bartter's syndrome. This defect is a marker for the syndrome and, presumably, is the cause of the supranormal tubular secretion of potassium that characterizes the disorder. The potassium depletion that results from excessive potassium excretion is probably the stimulus for the increased synthesis of prostacyclin by blood vessels and prostaglandin E2 by kidneys that occurs in Bartter's syndrome. The overproduction of prostaglandins mediates hyperreninemia, supranormal plasma bradykinin, supranormal plasma norepinephrine and vascular resistance to the pressor effects of angiotensin II and norepinephrine; treatment with a prostaglandin synthetase inhibitor corrects these abnormalities. Increases in angiotensin II and in norepinephrine appear to be compensatory changes, occurring in response to vasodilatation induced by vascular prostaglandins to maintain blood pressure. The hyperreninemia also stimulates production of aldosterone with aggravation of potassium loss.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0023-2173
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
60
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1212-4
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
The role of chloride transport in the thick ascending limb in the pathogenesis of Bartter's syndrome.
pubmed:publicationType
Journal Article