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(Circulation. 1999;99:468-471.)
© 1999 American Heart Association, Inc.

Editorials

Appreciating -Adrenergic Receptors and Their Role in Ischemic Left Ventricular Dysfunction

Morton J. Kern, MD

From the Department of Internal Medicine, Division of Cardiology, Saint Louis University Hospital, St Louis, Mo.

Correspondence to Morton J. Kern, MD, Director, J.G. Mudd Cardiac Catheterization Laboratory, Saint Louis University Hospital, 3635 Vista Ave at Grand Blvd, St Louis, MO 63110. E-mail kernm@slu.edu

Key Words: Editorials • receptors, adrenergic, alpha • ventricles

Understanding the role of -adrenergic receptors in the relationship between myocardial ischemia and left ventricular functional impairment is difficult and substantially more complex than simply producing a reduction in myocardial supply relative to the demand. Traditionally and in an oversimplified manner, ₁-adrenergic and postsynaptic adrenergic receptors are considered equivalent and mediate vasoconstriction. ₂-Adrenergic and presynaptic adrenergic receptors likewise are thought to be identical and mediate inhibition of sympathetic neural terminal release of norepinephrine. Further subtypes of ₁-,₂-adrenergic receptor subtype classifications (_1A, _1E, _2A, etc) exist but remain predominantly theoretical. Under normal conditions, -adrenergic vasoconstriction regulates metabolically induced coronary vasodilation to match oxygen supply to myocardial demand.¹ Under ischemic conditions, -adrenergic receptor stimulation may produce excess oxyradical production and calcium overload and release endothelial factors,^{2 3} theoretically and paradoxically potentiating myocardial ischemia. As clinicians, the difficulty in our understanding arises because of the many different experimental models and available -adrenergic receptor agonists and antagonists (Table 1). Heusch⁴ expertly identifies the controversial aspects of -adrenergic receptor activation, especially under conditions of ischemia, when this generally minor mediator becomes powerful enough to limit coronary blood flow when coronary vasodilatory reserve becomes exhausted. The potentially conflicting -adrenergic receptor responses can be inferred, in part, by response variances among anatomic locations (Table 2).

View this table: [in this window] [in a new window]   Table 1. Classification of -Adrenergic Receptor Subtypes in the Heart

View this table: [in this window] [in a new window]   Table 2. -Adrenergic Receptors and Left Ventricular Function

Additional complexity is added in conditions under which brief periods of myocardial ischemia, not resulting in myonecrosis, may be followed by . . . [Full Text of this Article]

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