Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1995-8-11
pubmed:abstractText
A sympathetic overactivity plays a major role in the pathogenesis of cardiovascular diseases in Westernized affluent societies. Of importance is an increased caloric intake and psychosocial stress which are associated with a raised central sympathetic outflow and unfavourable changes in metabolic parameters. Normalization of central sympathetic outflow could thus be a major therapeutic target. The newly developed antihypertensive drugs moxonidine and rilmenidine reduce the excitatory activity of neurons of the rostral ventrolateral medulla (RVLM) via binding to imidazoline receptors. Using radio telemetry, it is shown that, in contrast to the first generation centrally acting drug clonidine, moxonidine did not result in rebound of blood pressure after drug withdrawal in rats with spontaneous hypertension. In accordance, moxonidine is characterized by a low affinity for alpha-adrenoceptors and exhibits few side-effects. It is proposed that normalization of central sympathetic outflow represents a causal approach for improving crucial features of the metabolic syndrome.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0306-9877
pubmed:author
pubmed:issnType
Print
pubmed:volume
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
217-25
pubmed:dateRevised
2008-8-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Excess catecholamines and the metabolic syndrome: should central imidazoline receptors be a therapeutic target?
pubmed:affiliation
Molecular Cardiology Laboratory, University of Marburg, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't