Linked Life Data

10090325

Source:http://linkedlifedata.com/resource/pubmed/id/10090325

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-5-20
pubmed:abstractText
The effects of angiotensin converting enzyme inhibition and angiotensin II receptor blockade on the development of cardiac hypertrophy and myocardial insulin-like growth factor I (IGF-I) in volume overload were studied in male Wistar rats with aorto-caval fistulas (ACF). Rats were treated with ramipril (RAM, 3 mg kg(-1) day(-1)) for 4-20 days or losartan (LOS, 10 mg kg(-1) day(-1)) for 2-7 days. Myocardial IGF-I and IGF-I receptor (IGF-I-R) mRNA were determined by solution hybridization. ACF caused hypertrophy of left (LV) and right ventricles (RV). Hypertrophy appeared on day 2 and reached maximal values of +60% in LV and +75% in RV at day 12. Systolic blood pressure was initially reduced 15% but recovered by day 12. RAM abolished the recovery of blood pressure. Furthermore, RAM attenuated RV hypertrophy by 17% on day 7 and on day 20, RV weights were close to values found in controls. Beginning on day 9, RAM reduced LV weight back to control levels in parallel to blood pressure. In contrast, LOS affected neither RV nor LV hypertrophy. RV IGF-I mRNA increased 60-100% on day 7 alone in RV in ACF. RAM potentiated the increase in RV IGF-I to +400% and induced an increase in RV IGF-I-R mRNA on day 7 (+90%) in ACF. LOS did not affect RV IGF-I. Development of cardiac hypertrophy in ACF seemed independent of angiotensin II. RV hypertrophy was associated with activation of IGF-I independent of the renin-angiotensin system. IGF-I was further potentiated when development of hypertrophy was attenuated, possibly indicative of a greater urge for compensational growth in a relatively thinner and more volume-distended chamber.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0001-6772
pubmed:author
pubmed:issnType
Print
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
143-54
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10090325-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:10090325-Animals, pubmed-meshheading:10090325-Antihypertensive Agents, pubmed-meshheading:10090325-Aorta, Abdominal, pubmed-meshheading:10090325-Aortic Diseases, pubmed-meshheading:10090325-Arteriovenous Fistula, pubmed-meshheading:10090325-Cardiomegaly, pubmed-meshheading:10090325-Disease Models, Animal, pubmed-meshheading:10090325-Follow-Up Studies, pubmed-meshheading:10090325-Hemodynamics, pubmed-meshheading:10090325-Insulin-Like Growth Factor I, pubmed-meshheading:10090325-Losartan, pubmed-meshheading:10090325-Male, pubmed-meshheading:10090325-Myocardium, pubmed-meshheading:10090325-Pilot Projects, pubmed-meshheading:10090325-RNA, Messenger, pubmed-meshheading:10090325-Ramipril, pubmed-meshheading:10090325-Rats, pubmed-meshheading:10090325-Rats, Wistar, pubmed-meshheading:10090325-Receptor, IGF Type 1, pubmed-meshheading:10090325-Renin-Angiotensin System, pubmed-meshheading:10090325-Vena Cava, Inferior
pubmed:year
1999
pubmed:articleTitle
Interaction between the renin-angiotensin system and insulin-like growth factor I in aorto-caval fistula-induced cardiac hypertrophy in rats.
pubmed:affiliation
Department of Physiology, Institute of Physiology and Pharmacology and Research Center for Endocrinology and Metabolism, Göteborg University, Sweden.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't