کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2850154 | 1167749 | 2006 | 9 صفحه PDF | دانلود رایگان |
Compelling evidence now exists that proves adrenergic blockade is at the center of neurohormonal antagonism in heart failure (HF). Catecholamines are well known to act through both β- and α-adrenergic receptors (ARs), which mediate their effects through distinct receptor pathways. β-AR blockers are commonly used in the treatment of HF and have distinct receptor affinity profiles. The recent COMET trial comparing 2 important β-blocking drugs showed a distinct advantage for carvedilol in decreasing the risk of mortality from HF. The mechanism of action for carvedilol differs from metoprolol tartrate in its ability to block both α- and β-ARs, leading to renewed interest in the potential role of α-ARs in the progression of HF. In contrast, however, the ALLHAT study discontinued use of doxazosin, an α1-receptor blocker because of an increase in cardiovascular events among patients using this drug. The results of these studies appear to be in contrast with respect to the role of α-ARs in regards to cardiovascular pathophysiology. Further study of the α-receptor and understanding the role of α-ARs in HF is necessary to understand the therapeutic effect of α-blockade. This article reviews our understanding of the α-AR in HF.
Journal: American Heart Journal - Volume 152, Issue 5, November 2006, Pages 842–850