Linked Life Data

6318223

Source:http://linkedlifedata.com/resource/pubmed/id/6318223

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1984-2-24
pubmed:abstractText
To test the hypothesis that beta-blockade might impair potassium (K) tolerance in terminal renal failure we gave propranolol, and then atenolol, to a group of 12 clinically stable non-diabetic patients on chronic haemodialysis and on a constant diet containing approximately 50 mEq of K/day. Propranolol, 60 to 80 mg/day for 10 days induced a significant increase in predialysis serum K from 5.1 +/- 0.1 to 5.8 +/- 0.2 mEq/L (p less than 0.005). Atenolol (50 mg/day for 10 days) in the same group of patients did not produce a significant change in predialysis serum K (5.5 +/- 0.2 vs 5.2 +/- 0.2 mEq/L). Both propranolol and atenolol decreased heart rate but neither drug induced significant changes in plasma aldosterone, arterial pH, serum insulin or blood glucose. Thus in haemodialysis patients, beta-2 adrenergic blockade by propranolol is associated with a significant increase in serum K not mediated by pH, aldosterone or insulin, and probably due to inhibition of intracellular K uptake. Selective beta-1 adrenergic blockade by atenolol at low doses does not change serum K, and therefore, if indicated, cardioselective beta-blockers might be preferable to nonselective drugs in haemodialysis patients.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0071-2736
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
572-6
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Increase in serum potassium caused by beta-2 adrenergic blockade in terminal renal failure: absence of mediation by insulin or aldosterone.
pubmed:publicationType
Journal Article, Comparative Study