Role of cardiac renin-angiotensin system in the development of pressure-overload left ventricular hypertrophy in rats with abdominal aortic constriction

1996 ◽  
Vol 155 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Doodipala S. Reddy ◽  
Manjeet Singh ◽  
Sujata Ghosh ◽  
N. K. Ganguly
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Aortic Constriction ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Abdominal Aortic

Renin-angiotensin system and sympathetic nervous system in cardiac pressure-overload hypertrophy

2000 ◽  
Vol 279 (6) ◽  
pp. H2797-H2806 ◽  
Author(s):  
Wendell S. Akers ◽  
Andrew Cross ◽  
Robert Speth ◽  
Linda P. Dwoskin ◽  
Lisa A. Cassis
Keyword(s):  
Left Ventricle ◽  
Adrenergic Receptor ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Receptor Density ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Sympathetic Nervous

Angiotensin II and norepinephrine (NE) have been implicated in the neurohumoral response to pressure overload and the development of left ventricular hypertrophy. The purpose of this study was to determine the temporal sequence for activation of the renin-angiotensin and sympathetic nervous systems in the rat after 3–60 days of pressure overload induced by aortic constriction. Initially on pressure overload, there was transient activation of the systemic renin-angiotensin system coinciding with the appearance of left ventricular hypertrophy ( day 3). At day 10, there was a marked increase in AT1 receptor density in the left ventricle, increased plasma NE concentration, and elevated cardiac epinephrine content. Moreover, the inotropic response to isoproterenol was reduced in the isolated, perfused heart at 10 days of pressure overload. The affinity of the β2-adrenergic receptor in the left ventricle was decreased at 60 days. Despite these alterations, there was no decline in resting left ventricular function, β-adrenergic receptor density, or the relative distribution of β1- and β2-receptor sites in the left ventricle over 60 days of pressure overload. Thus activation of the renin-angiotensin system is an early response to pressure overload and may contribute to the initial development of cardiac hypertrophy and sympathetic activation in the compensated heart.

Lack of Association of the Renin-angiotensin System Genes Polymorphisms and Left Ventricular Hypertrophy in Hypertension

2001 ◽  
Vol 10 (3) ◽  
pp. 135-141 ◽  
Author(s):  
Eugene V. Shlyakhto ◽  
Eugene I. Shwartz ◽  
Yulia. B. Nefedova ◽  
Anna. V. Zukova ◽  
Tatyana. A. Vinnic ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Angiotensin System ◽  
Renin Angiotensin

Hydrochlorothiazide and alternative diuretics versus renin–angiotensin system inhibitors for the regression of left ventricular hypertrophy

2018 ◽  
Vol 36 (6) ◽  
pp. 1247-1255 ◽  
Author(s):  
George C. Roush ◽  
Ramy Abdelfattah ◽  
Steven Song ◽  
John B. Kostis ◽  
Michael E. Ernst ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Angiotensin System ◽  
Renin Angiotensin
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