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Am J Physiol Heart Circ Physiol 275: H534-H541, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 2, H534-H541, August 1998

ANG II-related myocardial damage: role of cardiac sympathetic catecholamines and beta -receptor regulation

Jeffrey R. Henegar, Dean D. Schwartz, and Joseph S. Janicki

Department of Physiology and Pharmacology, Auburn University, Auburn, Alabama 36849

The objectives of this study were 1) to determine whether ANG II-induced myocardial damage (ANG Dam) is mediated via the beta 1-adrenergic receptor, 2) to elucidate whether adrenal medulla or cardiac sympathetic neuron catecholamines are responsible for ANG Dam, and 3) to determine whether the lack of damage after 3 days of elevated ANG II levels is due to beta 1-receptor downregulation. To this end, ANG II was administered to rats 1) that were treated with a beta -receptor blocker, 2) after adrenal medullectomy and/or cardiac sympathectomy, and 3) for 3 or 8 days. ANG II caused both myocyte necrosis and coronary vascular damage after adrenal medullectomy but not after cardiac sympathectomy. There was a 38 and 55% decrease in beta -receptor density after 3 and 8 days, respectively, of ANG II infusion, and an upregulation to control levels 5 days after a 3-day ANG II infusion was stopped. We conclude that cardiac sympathetic neuron catecholamines are responsible for ANG Dam and that the acute nature of this damage is associated with a downregulation of beta 1-adrenergic receptors.

myocyte necrosis; atenolol; adrenal medullectomy; cardiac sympathectomy; coronary arteriolar damage


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