Renin-angiotensin system and sympathetic nervous system in cardiac pressure-overload hypertrophy
| Autor: | Robert C. Speth, Wendell S. Akers, Linda P. Dwoskin, Andrew M. Cross, Lisa A. Cassis |
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| Rok vydání: | 2000 |
| Předmět: |
Male
Sympathetic nervous system medicine.medical_specialty Sympathetic Nervous System Physiology Adrenergic beta-Antagonists Left ventricular hypertrophy Receptor Angiotensin Type 2 Receptor Angiotensin Type 1 Muscle hypertrophy Iodine Radioisotopes Rats Sprague-Dawley Renin-Angiotensin System Norepinephrine Physiology (medical) Internal medicine Receptors Adrenergic beta Renin–angiotensin system Ventricular Pressure medicine Animals Iodocyanopindolol Aorta Pressure overload Receptors Angiotensin business.industry Angiotensin II Myocardium Imidazoles medicine.disease Rats Autonomic nervous system medicine.anatomical_structure Endocrinology Echocardiography Ventricular pressure Hypertrophy Left Ventricular Cardiology and Cardiovascular Medicine business |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 279:H2797-H2806 |
| ISSN: | 1522-1539 0363-6135 |
| DOI: | 10.1152/ajpheart.2000.279.6.h2797 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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