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  Vol. 158 No. 4, February 23, 1998 TABLE OF CONTENTS
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Sulfonylureas and Ischemic Heart Disease

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Readers of Dagogo-Jack and Santiago's1 excellent review of type 2 diabetes may be unaware that the embers of controversy regarding the effects of sulfonylureas on the heart in patients with type 2 diabetes, originally raised by the much maligned University Group Diabetes Program study,2 have been fanned by a series of basic science and animal experiments conducted over the past decade.3

Briefly, sulfonylureas bind to specific membrane receptors on the beta cell causing membrane depolarization by closing the adenosine triphosphate–dependent potassium channel (KATP),4 thereby permitting an increase in intracellular calcium that leads to insulin secretion. The sulfonylurea receptor is a member of the adenosine triphosphate–binding family of receptors, and similar receptors are in the heart.5 Acute myocardial ischemia results in opening of KATPchannels with a reduction in calcium influx and a resultant decrease in myocardial contractility, which may protect the heart by reducing oxygen demand.6 Furthermore, brief ischemic . . . [Full Text of this Article]



THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

Acute Pancreatitis Associated with Celecoxib
Baciewicz et al.
ANN INTERN MED 2000;132:680-680.
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