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[Beta adrenergic receptors and experimental left ventricular hypertrophy]
J M Sénard1, M Galinier, P Valet
1Laboratoire de pharmacologie médicale et clinique, INSERM U 317, Faculté de médecine, Toulouse.
Archives Des Maladies Du Coeur Et Des Vaisseaux
|August 1, 1992
Summary
Sinoaortic denervation (SAD) in dogs leads to increased heart weight and left ventricular thickness, with elevated plasma catecholamines and reduced beta-adrenergic receptors. These effects normalize 18 months post-SAD, indicating cardiac adaptation.
Area of Science:
- Cardiovascular Physiology
- Neuroendocrinology
Context:
- Sinoaortic denervation (SAD) disrupts baroreceptor reflexes, impacting autonomic control of the cardiovascular system.
- Understanding the long-term cardiac and neurochemical adaptations following SAD is crucial for cardiovascular research.
Purpose:
- To investigate the effects of SAD on left ventricular hypertrophy, myocardial beta-adrenergic receptor density, and plasma catecholamine levels in normotensive and hypertensive dogs.
- To evaluate the temporal changes in these parameters at 1 and 18 months after SAD.
Summary:
- SAD induced significant increases in heart weight and left ventricular thickness in dogs.
- Plasma levels of noradrenaline and adrenaline were elevated post-SAD but normalized by 18 months.
- Myocardial beta-adrenergic receptor density (Bmax) was significantly reduced 1 month after SAD, returning to normal levels by 18 months.
Impact:
- This study reveals that sinoaortic denervation causes cardiac remodeling and alters beta-adrenergic signaling, with a notable capacity for normalization over time.
- Findings provide insights into the autonomic nervous system's role in regulating cardiac structure and function, particularly in response to baroreceptor dysfunction.