Key result
Beta-blockade prevented most ANG II-related myocyte necrosis and coronary vascular damage, suggesting damage is mediated by local neural catecholamines rather than elevated serum norepinephrine.
Beta-blockade prevents ANG II-induced myocyte and coronary vascular damage, suggesting that local neural catecholamine release rather than circulating norepinephrine is responsible for the early damage.
Does not support clinical use of beta-blockade for ANG II cardiac injury; hypothesis-generating for local neural catecholamine mechanisms in humans.
Acute elevations in circulating angiotensin II (ANG II) are known to increase circulating norepinephrine (NE) levels. However, the time course of catecholamine release relative to chronic ANG II infusion is not known. Furthermore, it is unknown if this ANG II-induced catecholamine release is ANG II type 1 (AT1) receptor mediated or whether the increase in serum catecholamines is responsible for the myocyte and coronary vascular damage seen within the first 3 days of chronic ANG II infusion. Therefore, we examined the influence of chronic ANG II stimulation on serum catecholamine levels with and without AT1 blockade and the effect of beta-blockade on ANG II-induced myocyte and coronary vascular damage. The results indicate that NE release is AT1 mediated, but NE is not significantly elevated until day 4 of ANG II infusion after which it remains elevated. beta-Blockade prevented most ANG II-related myocyte necrosis and coronary vascular damage. Therefore, myocyte and coronary vascular damage do not appear to be related to increased serum NE levels, but instead may be due to the release of neural catecholamines within the heart.
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Henegar et al. (1995) studied ANG II-induced myocyte and coronary vascular damage. Chronic ANG II infusion with AT1 blockade or beta-blockade vs. Chronic ANG II infusion alone was evaluated on Serum catecholamine levels and myocyte/coronary vascular damage. Beta-blockade prevented most ANG II-related myocyte necrosis and coronary vascular damage, suggesting damage is mediated by local neural catecholamines rather than elevated serum norepinephrine.
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