Related Experiment Videos
Left ventricular hypertrophy and arterial blood pressure in experimental models of hypertension
A F Dominiczak1, A M Devlin, M J Brosnan
1Department of Medicine and Therapeutics, Gardiner Institute Western Infirmary, Glasgow.
Insights
Cardiac hypertrophy is complex, influenced by more than just blood pressure. Genetic factors and the renin-angiotensin system play significant roles in left ventricular hypertrophy (LVH).
Area of Science:
- Cardiovascular Research
- Genetics
- Hypertension
Background:
- Cardiac hypertrophy was initially linked solely to increased pressure load in hypertension.
- The relationship between blood pressure and left ventricular (LV) mass is complex, not a simple dose-response.
- Non-hemodynamic factors, including genetic and neuro-hormonal influences, significantly impact LV mass.
Purpose of the Study:
- To investigate the multifaceted factors contributing to cardiac hypertrophy beyond pressure overload.
- To explore the roles of the renin-angiotensin system and genetic susceptibility in left ventricular hypertrophy (LVH).
Main Methods:
- Pharmacological studies on the regression or prevention of LVH.
- Experimental studies to induce LVH in normotensive strains.
- Genetic analyses, including co-segregation and genome scan studies.
Main Results:
- Hemodynamic factors are important, but non-hemodynamic influences are also critical.
- The renin-angiotensin system and its interplay with nitric oxide significantly affect LVH.
- Genetic strategies suggest the existence of specific "susceptibility genes" for LV hypertrophy.
Conclusions:
- Cardiac hypertrophy in hypertension is multifactorial, involving both hemodynamic and non-hemodynamic pathways.
- Genetic predisposition plays a crucial role in the development of LVH.
- Further research into "susceptibility genes" is warranted for essential hypertension.
Abstract:
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.