Linked Life Data

9495257

Source:http://linkedlifedata.com/resource/pubmed/id/9495257

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1998-3-19
pubmed:abstractText
Inhibition of the renin-angiotensin system has been shown to improve symptoms and prognosis in heart failure. We compared the effects of inhibition of angiotensin-converting enzyme or blockade of angiotensin II type 1 (AT1) receptors in a model with renin-induced hypertension that is known to exhibit similar changes in sympathetic activation and beta-adrenergic desensitization, as observed in heart failure. Treatment with captopril (100 mg/kg of feed) or the AT1-antagonist Bay 10-6734 (100 mg/kg of feed) was performed in transgenic rats harboring the mouse renin 2d gene [TG(mREN2)27]. Neuropeptide Y and angiotensin II levels, adenylyl cyclase activity, beta-adrenergic receptors, G(salpha), and G(ialpha) were investigated. TG(mREN2)27 showed a depletion of myocardial neuropeptide Y stores and an increase in myocardial angiotensin II concentrations. Isoprenaline- and guanylylimidodiphosphate-stimulated adenylyl cyclase activities and beta-adrenergic receptor density were reduced, whereas the catalyst and G(salpha)-function were unchanged. G(ialpha) protein and mRNA concentrations were increased. All alterations were normalized by both treatments. Systolic left ventricular pressures, plasma atrial natriuretic peptide, and myocardial steady state atrial natriuretic peptide mRNA concentrations and heart weights were similarly reduced by both treatments. Sympathetic neuroeffector defects are similarly reversed by angiotensin-converting enzyme inhibition or AT1 antagonism. The data support the concept that pharmacological interventions in the myocardial renin-angiotensin system significantly reverse local sympathetic neuroeffector defects. This could be important for the beneficial effects of these agents.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0194-911X
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
747-54
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9495257-Adenylate Cyclase, pubmed-meshheading:9495257-Angiotensin II, pubmed-meshheading:9495257-Angiotensin Receptor Antagonists, pubmed-meshheading:9495257-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:9495257-Animals, pubmed-meshheading:9495257-Animals, Genetically Modified, pubmed-meshheading:9495257-Atrial Natriuretic Factor, pubmed-meshheading:9495257-Blood Pressure, pubmed-meshheading:9495257-GTP-Binding Proteins, pubmed-meshheading:9495257-Heart, pubmed-meshheading:9495257-Hypertension, pubmed-meshheading:9495257-Myocardium, pubmed-meshheading:9495257-Neuropeptide Y, pubmed-meshheading:9495257-Organ Size, pubmed-meshheading:9495257-Rats, pubmed-meshheading:9495257-Rats, Sprague-Dawley, pubmed-meshheading:9495257-Receptor, Angiotensin, Type 1, pubmed-meshheading:9495257-Receptor, Angiotensin, Type 2, pubmed-meshheading:9495257-Receptors, Adrenergic, beta, pubmed-meshheading:9495257-Signal Transduction
pubmed:year
1998
pubmed:articleTitle
Effects of angiotensin II type 1 receptor blockade and angiotensin-converting enzyme inhibition on cardiac beta-adrenergic signal transduction.
pubmed:affiliation
Klinik III für Innere Medizin, Universität zu Köln, Germany. michael.boehm@medizin.uni-koeln.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't