Summary
Chronic, pathophysiological elevations of angiotensin (Ang) II cause myocyte necrosis and coronary vascular damage. These adverse effects are mediated by the angiotensin II type 1 (AT1) receptor and are, therefore, preventable with AT1 receptor blockade. Additionally, the intracellular signaling cascade stimulated by elevations in Ang II results in an AT1 receptor-mediated catecholamine release, and the myocardial damage can also be attenuated by β1-adrenergic receptor blockade. The restriction of myocardial damage to the first 3 days of Ang II infusion is due to subsequent downregulation of the β1-adrenergic receptor population. Discontinuation of the Ang II infusion results in a return to normal β1-adrenergic receptor density, which makes the myocardium susceptible once again to subsequent elevations of Ang II. This Ang II-related myocardial damage could play an important role in the pathogenesis of heart failure post-myocardial infarction or in other cardiac disease states.
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Henegar, J.R., Brower, G.L., Janicki, J.S. (1998). Characteristics and Mechanisms of Angiotensin II-Related Myocardial Damage. In: Dhalla, N.S., Zahradka, P., Dixon, I.M.C., Beamish, R.E. (eds) Angiotensin II Receptor Blockade Physiological and Clinical Implications. Progress in Experimental Cardiology, vol 2. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5743-2_37
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DOI: https://doi.org/10.1007/978-1-4615-5743-2_37
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