Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1998-2-17
pubmed:abstractText
Cardiac hypertrophy in essential and experimental (genetic) hypertension have been initially attributed to increased pressure load. However, the level of blood pressure does not parallel the degree of cardiac hypertrophy, i.e., a complex relationship rather than a simple dose-response effect has to be suggested. Several non-haemodynamic factors which influence LV mass have been identified with genetic and neuro-hormonal influences playing a major role. The experimental strategies which have been used to highlight one or more of these influences include pharmacological studies of regression or prevention of LVH and studies designed to produce LVH de-novo in normotensive strains. All these studies while confirming an important role of haemodynamic factors also stress the major influence of the renin-angiotensin system and the inter-relationship between angiotensin II and nitric oxide. In contrast, genetic strategies, from simple co-segregation analysis to most complex genome scan studies, suggest the existence of "susceptibility genes" for LV hypertrophy, a finding which deserves further study in large collections of siblings and family groups with essential hypertension.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0065-2598
pubmed:author
pubmed:issnType
Print
pubmed:volume
432
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
23-33
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Left ventricular hypertrophy and arterial blood pressure in experimental models of hypertension.
pubmed:affiliation
Department of Medicine and Therapeutics, Gardiner Institute Western Infirmary, Glasgow.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't